Most enzymes look ordinary. One does not.

One copy of SLCO1B1 c.521T>C. Higher myopathy risk on high-dose simvastatin.

CPIC and the FDA label treat this as decreased OATP1B1 function. Heterozygotes have several-fold higher risk of simvastatin-related muscle injury at 80 mg, and a smaller increase at 40 mg. Atorvastatin, pravastatin, rosuvastatin, and fluvastatin are preferred if a statin is indicated. This does not mean you cannot take a statin — it means the drug and dose should be chosen with this genotype in mind.

If a statin is ever prescribed, prefer non-simvastatin agents or keep simvastatin at a low dose. Mention this result to the prescriber.

No *2, *3, or *17. Standard clopidogrel bioactivation and standard PPI exposure.

rs4244285 G/G (not *2), rs4986893 G/G (not *3), rs12248560 C/C (not *17). Clopidogrel should form its active metabolite normally. This is the genotype CPIC treats as standard dosing for clopidogrel, voriconazole, and most CYP2C19 substrates.

No CYP2C9 *2 or *3. VKORC1 −1639 is G/G, the higher warfarin-dose haplotype.

rs9923231 C/C is the plus-strand equivalent of −1639G/G. Combined with CYP2C9 *1/*1 this is the typical European high-to-average dose cluster. Warfarin should still be INR-guided. The genotype mainly tells a prescriber not to start at a tiny dose.

Typical European genotype. Standard-to-lower tacrolimus requirements if a transplant were ever needed.

The C allele is *3 (splicing defect). CC means no functional CYP3A5. Most Europeans are *3/*3. Expressors (*1) need higher tacrolimus doses. No action unless immunosuppressants enter the picture.

No common TPMT *2/*3 or NUDT15 *3 alleles. Standard azathioprine / 6-MP starting point.

CPIC still recommends considering a clinical TPMT/NUDT15 test before thiopurines because rare alleles and assay confirmation matter. The common risk SNPs on this chip are wild-type.

*2A, *13, and c.2846A>T are absent. Standard fluoropyrimidine starting point if cancer chemo were needed.

These three variants explain a large share of severe 5-FU / capecitabine toxicity. Absence is good news but not a complete DPYD sequence. Oncology teams still use their own protocols.

The HCP5 tag for abacavir hypersensitivity is absent.

rs2395029 G tags HLA-B*5701. T/T is the non-risk call. Abacavir is still tested in clinic before use; this is consistent with a negative screen.

*1F/*1F. Coffee is cleared quickly. The caffeine–heart-attack interaction seen in slow metabolizers is less relevant.

A/A at rs762551 is the inducible fast phenotype, especially in smokers and heavy coffee drinkers. Fast metabolizers generally tolerate afternoon coffee better and do not show the same coffee–MI association reported for slow (*1A) metabolizers. Sleep still depends on timing and dose.

One *80-linked allele. Can mean mildly higher unconjugated bilirubin; irinotecan caution is usually for *28/*28.

rs887829 T is in near-perfect LD with UGT1A1*28 in Europeans. Heterozygotes sometimes have slightly higher baseline bilirubin (Gilbert spectrum) and do not usually need irinotecan dose cuts. Mention it if a chemistry panel shows isolated high bilirubin.

The *3 frameshift looks heterozygous. Microarrays cannot resolve CYP2D6 copy number, so this is a hint, not a star-allele call.

CYP2D6 metabolizes many antidepressants, atomoxetine, codeine, tamoxifen, and metoprolol. A single *3 would lean intermediate if the other allele is *1. Hybrid genes, deletions (*5), and duplications are invisible here. Do not change psychiatric or pain meds from this chip alone.

If a CYP2D6-sensitive drug is being started (codeine, tamoxifen, some SSRIs), a clinical PGx panel is the right test.

No A118G. Standard mu-opioid binding in most studies.

118G (Asp) has been tied to altered alcohol reward and slightly higher opioid-dose needs. A/A is Asn/Asn, the common form.