ALDH2: the alcohol flush
Your genotype · G/A → Reduced clearance, flush-prone
EU-sovereign · DNA re-analysis · made in Finland
Aimosti re-analyses a DNA file you already own, a sequenced genome or a 23andMe-style chip export, against current clinical and research databases. When the evidence shifts, we re-read your file and flag what changed.
Read on your device, not ours. Your file is never uploaded and no account is needed. We are a genomics company telling you not to send us your genome yet, and that is deliberate. Security & your data →
Reading on your device…
That's . We can build your report from it.
What it can tell you
What it can't
A chip reads a fixed set of common spots, so the rare-variant panels need a sequenced genome. We tell you this now rather than after you have paid.
One-time, yours to keep. Your file is still on your device: you upload it after checkout, over an encrypted connection, to storage in Finland.
That's : aligned reads.
This is exactly what the Deep Read pharmacogenomic panel needs: 29 targets read at base level, including the CYP2D6 star-alleles a normal VCF cannot reliably call. The standard report is built from a VCF/gVCF, so aligned reads sit alongside one rather than replacing it.
Deep Read needs standard-depth reads. A low-pass file, MyHeritage's own sequencing download among them, is read about twice over rather than thirty times, which is too thin to call these genes from. We measure the depth and stop rather than guess.
A CRAM also needs the exact reference assembly it was compressed against, not merely the same genome build. We hold the common ones and check yours before taking any money, so an assembly we cannot read is refused rather than charged for.
What the pair covers
The bundle is the whole-genome report plus the Deep Read panel. The report is built from a variant file and the panel from your reads, so it takes both. Most sequencing providers hand you both in the same download.
Nothing was uploaded, and you have not paid anything. We would rather turn a file away here than sell you a report it cannot support.
This check ran on your device from your file's header. We confirm the full file after upload, and never charge for a report we cannot build.
From €19 for a genotyping-array file (23andMe, AncestryDNA, MyHeritage, FamilyTreeDNA, LivingDNA), or €39 for whole-genome. One-time, yours to keep.
We keep your report current. Own every report forever. €29/yr keeps it updating. Stop anytime and you keep the last one. Never rented back to you.
Your data stays in Finland. Encrypted in transit, never sold, deleted on demand.
Every panel below is the real report engine over a made-up genome, the same one the sample walkthrough uses. Nothing here is a picture of the product.
How your genes can affect the way your body handles specific drugs.
No drugs or genes match your search.
ABCG2: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: Little to no typical activity, which can substantially change how affected medicines behave at a standard dose. A prescriber may adjust the choice or dose.
Increased rosuvastatin exposure compared to normal and decreased function; unknown myopathy risk; increased lipid-lowering effects CPIC's combined ABCG2+SLCO1B1 guidance, shown assuming SLCO1B1 is typical.
Per CPIC (A): "Prescribe ≤20mg as a starting dose and adjust doses of rosuvastatin based on disease-specific and specific population guidelines. If dose >20mg needed for desired efficacy, consider an alternative statin or combination therapy (i.e., rosuvastatin plus non-statin guideline directed medical therapy) (PMID: 30423391)."
CPIC CPIC snapshot 2026-06-13 · CPIC: ABCG2 (allele functionality, diplotype-phenotype, drug guidance)
CACNA1S: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: Associated with malignant hyperthermia, a serious reaction to certain anaesthetics. Make sure any anaesthetist knows before surgery.
Individuals are at increased risk of developing malignant hyperthermia if administered halogenated volatile anesthetics or the depolarizing muscle relaxant succinylcholine CPIC's combined CACNA1S+RYR1 guidance, shown assuming RYR1 is typical.
Per CPIC (A): "Halogenated volatile anesthetics or the depolarizing muscle relaxant succinylcholine are relatively contraindicated in persons with malignant hyperthermia susceptibility (MHS). They should not be used, except in extraordinary circumstances where the benefits outweigh the risks. In general, alternative anesthetics are widely available and effective in patients with MHS."
CPIC CPIC snapshot 2026-06-13 · CPIC: CACNA1S (allele functionality, diplotype-phenotype, drug guidance)
CYP2B6: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works slowly, so affected medicines can build up at a standard dose, sometimes meaning stronger effects or more side-effects. A prescriber may choose a lower dose or a different medicine.
Higher dose-adjusted trough concentrations of efavirenz compared with normal metabolizers; significantly increased risk of CNS adverse events and treatment discontinuation
Per CPIC (A): "Consider initiating efavirenz with decreased dose of 400 or 200 mg/day"
Greatly reduced metabolism of sertraline to less active compounds when compared to CYP2B6 normal metabolizers. Higher plasma concentrations may increase the probability of side effects. CPIC's combined CYP2B6+CYP2C19 guidance, shown assuming CYP2C19 is typical.
Per CPIC (B): "Consider a lower starting dose, slower titration schedule and 25% reduction of standard maintenance dose as compared to CYP2B6 normal metabolizers or select a clinically appropriate alternative antidepressant not predominantly metabolized by CYP2B6."
CPIC CPIC snapshot 2026-06-13 · CPIC: CYP2B6 (allele functionality, diplotype-phenotype, drug guidance)
CYP2C19: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works faster than typical, so affected medicines may be cleared more quickly than a standard dose assumes, worth a prescriber's awareness.
Increased metabolism of tertiary amines compared to normal metabolizers; Greater conversion of tertiary amines to secondary amines may affect response or side effects CPIC's combined CYP2C19+CYP2D6 guidance, shown assuming CYP2D6 is typical.
Per CPIC (A): "Consider alternative drug not metabolized by CYP2C19; If amitriptyline is warranted, utilize therapeutic drug monitoring to guide dose adjustment."
Increase in metabolism of citalopram and escitalopram to less active compounds when compared to CYP2C19 normal metabolizers. Lower plasma concentrations decrease the probability of clinical benefit.
Per CPIC (A): "Initiate therapy with recommended starting dose. If patient does not adequately respond to recommended maintenance dosing, consider titrating to a higher maintenance dose or switching to a clinically appropriate alternative antidepressant not predominantly metabolized by CYP2C19."
Increased metabolism of tertiary amines compared to normal metabolizers; Greater conversion of tertiary amines to secondary amines may affect response or side effects CPIC's combined CYP2C19+CYP2D6 guidance, shown assuming CYP2D6 is typical.
Per CPIC (B): "Consider alternative drug not metabolized by CYP2C19; If clomipramine is warranted, utilize therapeutic drug monitoring to guide dose adjustment."
Normal or increased clopidogrel active metabolite formation; normal or lower on-treatment platelet reactivity; no association with higher bleeding risk
Per CPIC (A): "If considering clopidogrel, use at standard dose (75 mg/day)"
Decreased plasma concentrations of PPIs compared to CYP2C19 NMs; increased risk of therapeutic failure
Per CPIC (B): "Initiate standard starting daily dose. Consider increasing dose by 50-100% for the treatment of H. pylori infection and erosive esophagitis. Daily dose may be given in divided doses. Monitor for efficacy."
Increased metabolism of tertiary amines compared to normal metabolizers; Greater conversion of tertiary amines to secondary amines may affect response or side effects CPIC's combined CYP2C19+CYP2D6 guidance, shown assuming CYP2D6 is typical.
Per CPIC (B): "Consider alternative drug not metabolized by CYP2C19; If doxepin is warranted, utilize therapeutic drug monitoring to guide dose adjustment."
Increased metabolism of tertiary amines compared to normal metabolizers; Greater conversion of tertiary amines to secondary amines may affect response or side effects CPIC's combined CYP2C19+CYP2D6 guidance, shown assuming CYP2D6 is typical.
Per CPIC (B): "Consider alternative drug not metabolized by CYP2C19; If imipramine is warranted, utilize therapeutic drug monitoring to guide dose adjustment."
Decreased plasma concentrations of PPIs compared to CYP2C19 NMs; increased risk of therapeutic failure
Per CPIC (A): "Initiate standard starting daily dose. Consider increasing dose by 50-100% for the treatment of H. pylori infection and erosive esophagitis. Daily dose may be given in divided doses. Monitor for efficacy."
Small increase in metabolism of sertraline to less active compounds when compared to CYP2C19 normal metabolizers. CPIC's combined CYP2C19+CYP2B6 guidance, shown assuming CYP2B6 is typical.
Per CPIC (A): "Initiate therapy with recommended starting dose."
Increased metabolism of tertiary amines compared to normal metabolizers; Greater conversion of tertiary amines to secondary amines may affect response or side effects CPIC's combined CYP2C19+CYP2D6 guidance, shown assuming CYP2D6 is typical.
Per CPIC (B): "Consider alternative drug not metabolized by CYP2C19; If trimipramine is warranted, utilize therapeutic drug monitoring to guide dose adjustment."
In patients for whom a rapid metabolizer genotype (*1/*17) is identified, the probability of attainment of therapeutic concentrations is modest with standard dosing
Per CPIC (A): "Choose an alternative agent that is not dependent on CYP2C19 metabolism as primary therapy in lieu of voriconazole. Such agents include isavuconazole, liposomal amphotericin B, and posaconazole."
CPIC CPIC snapshot 2026-06-13 · CPIC: CYP2C19 (allele functionality, diplotype-phenotype, drug guidance)
A liver enzyme that clears warfarin, several NSAIDs and phenytoin. Reduced-function variants slow that clearance.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works somewhat slower than typical, so affected medicines can build up a little at a standard dose, worth a prescriber's awareness.
Slower clearance generally predicts a lower stable dose and a higher early-bleeding risk.
CPIC: the genotype-guided warfarin algorithm (CYP2C9 + VKORC1 + clinical factors) applies; reduced function typically lowers the predicted dose.
Higher exposure to CYP2C9-cleared NSAIDs is possible.
CPIC: the guideline discusses starting at the lowest effective dose for affected NSAIDs and titrating to response.
CPIC CPIC (CYP2C9 activity score; warfarin 2017) · CPIC: warfarin, CYP2C9 & VKORC1 · PharmVar: CYP2C9 (nomenclature)
The most important drug-metabolising enzyme: it activates or clears codeine, tramadol, tamoxifen and roughly a quarter of common medications. Copy-number and paralog structure make it readable only from aligned reads.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works much faster than typical: some medicines are cleared quickly (a standard dose may be too low), and for a few 'prodrugs' (such as codeine) the body can make too much active drug. A prescriber should be aware.
Rapid conversion can produce unsafe active-opioid levels.
CPIC: the guideline suggests avoiding codeine/tramadol and using an analgesic not metabolised by CYP2D6.
Increased endoxifen formation.
CPIC: standard use per label.
CPIC CPIC (CYP2D6 allele functionality + activity score, 2021) · CPIC: CYP2D6 allele functionality & activity score · PharmVar: CYP2D6 (nomenclature)
DPYD: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works somewhat slower than typical, so affected medicines can build up a little at a standard dose, worth a prescriber's awareness.
Decreased DPD activity (leukocyte DPD activity at 30% to 70% that of the normal population) and increased risk for severe or even fatal drug toxicity when treated with fluoropyrimidine drugs
Per CPIC (A): "Reduce starting dose by 50% followed by titration of dose based on toxicity or therapeutic drug monitoring (if available)."
CPIC CPIC snapshot 2026-06-13 · CPIC: DPYD (allele functionality, diplotype-phenotype, drug guidance)
G6PD: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: Reduced G6PD activity, which raises the risk of red-blood-cell breakdown (haemolysis) with certain medicines and foods. Important to flag to a prescriber before those exposures.
Low-to-no risk of acute hemolytic anemia
Per CPIC (C): "No reason to avoid based on G6PD status at standard doses"
High risk of acute hemolytic anemia
Per CPIC (A): "Avoid use"
Medium risk of acute hemolytic anemia
Per CPIC (A): "Use at standard doses with caution and with close monitoring for anemia"
High risk of acute hemolytic anemia with standard (or higher than standard) anti-relapse dosages for Plasmodium vivax or Plasmodium ovale of 0.25-0.5 mg/kg daily for 14 days
Per CPIC (A): "Avoid primaquine, except in the following cases where established expert consensus guidelines for the treatment of malaria should be followed: (1) Treating Plasmodium vivax or Plasmodium ovale malaria for radical cure of liver-stage infections: 0.75 mg/kg once weekly x8 weeks (WHO) or 45 mg once weekly x8 weeks (CDC) - with close monitoring for hemolysis; (2) Treating Plasmodium falciparum malaria by using primaquine single dose as a gametocytocide at 0.25 mg/kg (WHO) - without need for monitoring for hemolysis."
CPIC CPIC snapshot 2026-06-13 · CPIC: G6PD (allele functionality, diplotype-phenotype, drug guidance)
NAT2: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works slowly, so affected medicines can build up at a standard dose, sometimes meaning stronger effects or more side-effects. A prescriber may choose a lower dose or a different medicine.
Predicted to have increased hydralazine plasma concentrations compared to NAT2 rapid and intermediate metabolizers, which may lead to both increased efficacy and adverse effects, including drug-induced systemic lupus erythematosus.
Per CPIC (A): "Initiate therapy at a total daily dose of 40 to 75 mg. Carefully titrate dose upward to clinical effect or guideline-recommended dose; use caution with total daily hydralazine doses of 200 mg or more."
CPIC CPIC snapshot 2026-06-13 · CPIC: NAT2 (allele functionality, diplotype-phenotype, drug guidance)
NUDT15: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works somewhat slower than typical, so affected medicines can build up a little at a standard dose, worth a prescriber's awareness.
Increased risk of thiopurine-related leukopenia, neutropenia and myelosuppression. CPIC's combined NUDT15+TPMT guidance, shown assuming TPMT is typical.
Per CPIC (A): "Initiate therapy with reduced starting doses (30-80% of standard starting dose) if standard starting dose is ≥2 mg/kg/day. If starting dose is already below standard starting dose, dose reduction might not be necessary. During therapy, adjust the doses of azathioprine based on the degree of myelosuppression and disease-specific guidelines. It usually takes at least 2-4 weeks of stable dosing to reach steady state after each dose adjustment."
Increased risk of thiopurine-related leukopenia, neutropenia and myelosuppression. CPIC's combined NUDT15+TPMT guidance, shown assuming TPMT is typical.
Per CPIC (A): "Initiate therapy with decreased starting doses (30-80% of standard starting dose) if starting dose is ≥75 mg/m2/day (for malignancy) or ≥1.5 mg/kg/day (for nonmalignancy). If starting dose is already below standard starting dose, dose reduction might not be necessary. During therapy, adjust mercaptopurine doses based on the degree of myelosuppression and disease-specific guidelines. It usually takes at least 2-4 weeks of stable dosing to reach steady state after each dose adjustment. If myelosuppression occurs, and the patient is on combination therapy, emphasis should be on reducing mercaptopurine over other agents."
Increased risk of thiopurine-related leukopenia, neutropenia and myelosuppression. CPIC's combined NUDT15+TPMT guidance, shown assuming TPMT is typical.
Per CPIC (A): "Initiate therapy with decreased starting doses (30-80% of standard starting dose) if standard starting dose is ≥40 mg/m2/day. If starting dose is already below standard starting dose, dose reduction might not be necessary. During therapy, adjust the doses of thioguanine based on the degree of myelosuppression and disease-specific guidelines. It usually takes at least 2-4 weeks of stable dosing to reach steady state after each dose adjustment. If myelosuppression occurs, and the patient is on combination therapy, emphasis should be on reducing thioguanine over other agents."
CPIC CPIC snapshot 2026-06-13 · CPIC: NUDT15 (allele functionality, diplotype-phenotype, drug guidance)
SLCO1B1: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: Little to no typical activity, which can substantially change how affected medicines behave at a standard dose. A prescriber may adjust the choice or dose.
Increased atorvastatin exposure as compared to normal and decreased function which may translate to increased myopathy risk.
Per CPIC (A): "Prescribe ≤20mg as a starting dose and adjust doses of atorvastatin based on disease-specific guidelines. If dose >20mg is needed for desired efficacy, consider rosuvastatin or combination therapy (i.e., atorvastatin plus non-statin guideline directed medical therapy) (PMID: 30423391)."
Increased fluvastatin exposure as compared to normal and decreased function; Typical myopathy risk with doses less ≤40 mg. CPIC's combined SLCO1B1+CYP2C9 guidance, shown assuming CYP2C9 is typical.
Per CPIC (A): "Prescribe ≤40mg per day as a starting dose and adjust doses of fluvastatin based on disease-specific guidelines. If patient is tolerating 40mg per day but higher potency is needed, a higher dose (>40mg) or an alternative statin or combination therapy (i.e. fluvastatin plus non-statin guideline directed medical therapy) (PMID: 30423391) could be considered. Prescriber should be aware of possible increased risk for myopathy with fluvastatin especially with doses >40mg per day."
Increased lovastatin acid exposure as compared to normal and decreased function which may translate to increased myopathy risk
Per CPIC (A): "Prescribe an alternative statin depending on the desired potency (see Figure 1 of PMID: 35152405 for recommendations for alternative statins)."
Increased pitavastatin exposure as compared to normal and decreased function which may translate to increased myopathy risk.
Per CPIC (A): "Prescribe ≤1mg as a starting dose and adjust doses of pitavastatin based on disease-specific guidelines. If dose >1mg needed for desired efficacy, consider an alternative statin (see Figure 1 of PMID: 35152405 for recommendations for alternative statins) or combination therapy (i.e. pitavastatin plus non-statin guideline directed medical therapy)(PMID: 30423391)."
Increased pravastatin statin exposure as compared to normal and decreased function; Typical myopathy risk with doses ≤40 mg.
Per CPIC (A): "Prescribe ≤40mg as a starting dose and adjust doses of pravastatin based on disease-specific guidelines. If patient is tolerating 40mg dose but higher potency is needed, a higher dose (>40mg) or an alternative statin (see Figure 1 of of [sic] PMID: 35152405 for recommendations for alternative statins) or combination therapy (i.e. pravastatin plus non-statin guideline directed medical therapy)(PMID: 30423391) could be considered. Prescriber should be aware of possible increased risk for myopathy especially with pravastatin doses >40mg."
Increased rosuvastatin exposure as compared to normal function and decreased function; Typical myopathy risk with doses ≤20 mg. CPIC's combined SLCO1B1+ABCG2 guidance, shown assuming ABCG2 is typical.
Per CPIC (A): "Prescribe ≤20mg as a starting dose and adjust doses of rosuvastatin based on disease-specific and specific population guidelines. If dose > 20mg needed for desired efficacy, consider combination therapy (i.e., rosuvastatin plus non-statin guideline directed medical therapy) (PMID: 30423391)."
Increased simvastatin acid exposure compared to normal and decreased function; highly increased myopathy risk
Per CPIC (A): "Prescribe an alternative statin depending on the desired potency (see Figure 1 of PMID: 35152405 for recommendations for alternative statins)."
CPIC CPIC snapshot 2026-06-13 · CPIC: SLCO1B1 (allele functionality, diplotype-phenotype, drug guidance)
TPMT: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works somewhat slower than typical, so affected medicines can build up a little at a standard dose, worth a prescriber's awareness.
TPMT IMs have moderate to high erythrocyte concentrations of TGN metabolites and low concentrations of MeMPNs compared to TPMT NMs. CPIC's combined TPMT+NUDT15 guidance, shown assuming NUDT15 is typical.
Per CPIC (A): "Initiate therapy with reduced starting doses (30-80% of standard starting dose) if standard starting dose is ≥2 mg/kg/day. If starting dose is already below standard starting dose, dose reduction might not be necessary. During therapy, adjust the doses of azathioprine based on the degree of myelosuppression and disease-specific guidelines. It usually takes at least 2-4 weeks of stable dosing to reach steady state after each dose adjustment."
TPMT IMs have moderate to high erythrocyte concentrations of TGN metabolites and low concentrations of MeMPNs compared to TPMT NMs when receiving standard dose. CPIC's combined TPMT+NUDT15 guidance, shown assuming NUDT15 is typical.
Per CPIC (A): "Initiate therapy with decreased starting doses (30-80% of standard starting dose) if starting dose is ≥75 mg/m2/day (for malignancy) or ≥1.5 mg/kg/day (for nonmalignancy). If starting dose is already below standard starting dose, dose reduction might not be necessary. During therapy, adjust mercaptopurine doses based on the degree of myelosuppression and disease-specific guidelines. It usually takes at least 2-4 weeks of stable dosing to reach steady state after each dose adjustment. If myelosuppression occurs, and the patient is on combination therapy, emphasis should be on reducing mercaptopurine over other agents."
TPMT IMs have moderate to high erythrocyte concentrations of TGN metabolites compared to TPMT NMs. CPIC's combined TPMT+NUDT15 guidance, shown assuming NUDT15 is typical.
Per CPIC (A): "Initiate therapy with decreased starting doses (30-80% of standard starting dose) if standard starting dose is ≥40 mg/m2/day. If starting dose is already below standard starting dose, dose reduction might not be necessary. During therapy, adjust the doses of thioguanine based on the degree of myelosuppression and disease-specific guidelines. It usually takes at least 2-4 weeks of stable dosing to reach steady state after each dose adjustment. If myelosuppression occurs, and the patient is on combination therapy, emphasis should be on reducing thioguanine over other agents."
CPIC CPIC snapshot 2026-06-13 · CPIC: TPMT (allele functionality, diplotype-phenotype, drug guidance)
UGT1A1: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: This enzyme works somewhat slower than typical, so affected medicines can build up a little at a standard dose, worth a prescriber's awareness.
Somewhat decreased UGT1A1 activity; low likelihood of bilirubin-related discontinuation of atazanavir.
Per CPIC (A): "There is no need to avoid prescribing of atazanavir based on UGT1A1 genetic test result. Inform the patient that some patients stop atazanavir because of jaundice (yellow eyes and skin), but that this patient's genotype makes this unlikely (less than about a 1 in 20 chance of stopping atazanavir because of jaundice)."
CPIC CPIC snapshot 2026-06-13 · CPIC: UGT1A1 (allele functionality, diplotype-phenotype, drug guidance)
CYP3A5: CPIC pharmacogenomic guidance, restated. Phenotype is keyed by the called diplotype; drug guidance is CPIC's, quoted and attributed.
from your aligned reads · PyPGx 0.26.0
In plain terms: Typical activity for this enzyme: standard prescribing assumptions usually apply for the medicines below.
Lower dose-adjusted trough concentrations of tacrolimus and decreased chance of achieving target tacrolimus concentrations.
Per CPIC (A): "Increase starting dose 1.5 to 2 times recommended starting dose. Total starting dose should not exceed 0.3 mg/kg/day. Use therapeutic drug monitoring to guide dose adjustments."
CPIC CPIC snapshot 2026-06-13 · CPIC: CYP3A5 (allele functionality, diplotype-phenotype, drug guidance)
Your ancestry composition, with a range on every component. The map is the one your report draws.
Drawing the map
29 pharmacogenes read from the BAM, each with how much of the gene the reads could call.
29 called0 indeterminate0 low coverage
CYP2D6 *1x2/*1 · Ultrarapid Metabolizer
CLN3 deletion, called from read depth · Juvenile neuronal ceroid lipofuscinosis (CLN3 / Batten disease) · heterozygous
TYROBP deletion, called from read depth · Nasu-Hakola disease (PLOSL) · two copies
What every panel sits on: 1,042 panel regions of GRCh38 · ClinVar 2026-07 lists 482,198 classified variants
Modules
Each module is anchored to an authoritative, version-pinned source. The speculative modules are walled off from the clinical ones, so curiosity never wears the authority of settled science.
Pathogenic / likely-pathogenic variants in an established actionable-gene panel, framed as personal risk, never a verdict.
A recessive-lens look at carrier variants in your file, for family planning, with the un-callable conditions named.
How your genotype may affect specific medicines, restating CPIC, to discuss with a prescriber.
Benign, well-replicated, genome-wide-significant traits that clear a strict evidence gate. No SNPedia folklore.
Your deep maternal and paternal lines as global haplogroups, one thread of your tree, never a "percent ancestry" figure.
Dozens of readings from the interesting edge of the science: alcohol-flush and caffeine metabolism, the natural short-sleeper genes, longevity curios, and the over-hyped classics we keep in to set the record straight (the “warrior gene”, the serotonin-transporter “depression gene”). Each one is labelled by how much it weighs.
The playful gene-quirks people love to look up (why coriander can taste of soap, red hair, spicy-food tolerance, even the genetics of rage at chewing sounds), labelled, bluntly, as for curiosity only.
Everyone else either hides the speculative stuff or sells it as gospel. We show dozens of the variants you actually want to see, each wearing a blunt evidence tier, from replicated down to contested.
Your genotype · G/A → Reduced clearance, flush-prone
+ NEW ClinVar reclassified a variant in your file to Likely pathogenic.
~ UPDATED A Frontier association gained a replication cohort.
· STABLE Everything else unchanged since your last report.
Databases improve every month. Keep just your small normalised variant file and its ancestry marker extract with us, never raw reads, and we silently re-match them as the literature moves, then tell you plainly what changed. Withdraw any time; your last report is always yours.
≈ €29 / year · raw reads never retained
Pick where to start. Every report is a one-time purchase you own forever. To keep it current as the science moves, add the re-analysis subscription for €29/yr. Compare plans →
For 23andMe, AncestryDNA, MyHeritage, FamilyTreeDNA, LivingDNA and similar genotyping-array exports: everything your chip can call, fully attributed. Carrier status and the full clinical panel need whole-genome data. MyHeritage kits sold since October 2025 may be sequenced rather than typed on an array, so check which file you have.
Grow into it: upgrade to the full WGS report for €20 whenever you’re ready.
Every module over your whole-genome file: the deepest read of the genome you already own.
The full clinical-findings panel and carrier status live here. A chip file cannot give you either.
What only aligned reads (the BAM or CRAM from your provider) can answer: CYP2D6 copy number, a per-gene callability map of exactly what we examined, two deletions called from depth and typed HLA-DQ, on top of the full 29-target pharmacogene panel.
Prepay Deep Read with the WGS bundle to save.
Promethease and Genetic Genie read the same public databases we do. The difference is time. They hand you a report frozen on the day you run it, read from the few hundred thousand positions a genotyping chip types. We read your whole genome where you have it, attribute every finding to the guideline it came from, and can re-read your file as those guidelines change. Your report is a one-off purchase and stays yours. Keeping it current as the guidelines move is the optional re-analysis subscription, and you can start or stop that whenever you like.
Named services are described from their public product pages; features change and we don't speak for them. Three years later, that report still says exactly what it said on the day you ran it.
No. Aimosti never takes a sample or sequences anything. You bring whole-genome data you already had produced; we re-analyse the variant file.
No. Every finding is a literature match against public databases: information to discuss with a clinician and confirm with a validated gene test. It is never a diagnosis or medical advice.
A whole-genome gVCF gives the most complete report: it records which regions your sequencing covered, so "not found" can mean "examined and clear" rather than merely absent. A plain VCF also gives the full report, read as variant-only. Nebula Genomics, Dante Labs, Sequencing.com and the like are good to go. Several of them, Nebula, Gencove and Dante among them, only ship a variant-only VCF; that still gives the full report, so upload what you have. Check which depth you bought, though: a whole-genome product can be sold at 1x or 2x as well as at 30x. A low-pass genome is imputed against a reference panel rather than read directly, which is good for ancestry, traits and pharmacogenomics and cannot carry the clinical-findings and carrier panels, so it is the €19 report rather than the €39 one. Genotyping-array raw data from 23andMe, AncestryDNA, MyHeritage, FamilyTreeDNA or LivingDNA works too, for a lighter report (traits, pharmacogenomics and ancestry); clinical findings and carrier status need a sequenced genome. MyHeritage kits sold since October 2025 are sequenced rather than typed on a chip, and the raw-data export they hand you still works here.
Stored in Finland (Helsinki), never leaving the EU, never sold or mined, deleted on demand. Security & your data →
One living report, many modules. Read in Finland, attributed to the source, yours to keep.
Get your report · €39