What you carry at this position in your DNA and what research says about it.
Statin Side Effect Risk: 10/10 evidence, 118 publications.
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Sample genotype (not yours): T/T
Typical Statin Tolerance and Normal Drug Clearance
Normal transporter function ensures that cholesterol-lowering medications are processed safely. The risk of developing severe muscle pain or weakness from statin therapy is very low.
What this genotype means: Normal statin metabolism; Typical risk of muscle side effects; Standard drug clearance rates.
Sample genotype (not yours): C/C
Highly Elevated Risk of Statin Muscle Damage
Two copies of the C allele severely impair liver transporter function, leading to high blood levels of certain medications. This significantly increases the risk of severe statin-induced muscle pain and toxicity.
What this genotype means: Severely reduced statin clearance; Up to 17-fold higher risk of muscle toxicity; Significantly slower methotrexate processing.
Sample genotype (not yours): T/C
Moderately Increased Risk of Statin Muscle Pain
One copy of the C allele reduces liver transporter activity, causing certain medications to build up in the blood. This moderately raises the likelihood of experiencing statin-induced muscle pain or weakness.
What this genotype means: Slower clearance of certain statins; Higher risk of statin-induced muscle pain; Altered processing of methotrexate.
Gene function and biological role
Gene Function: The SLCO1B1 gene encodes a crucial transport protein called organic anion transporting polypeptide 1B1, or OATP1B1 [1]. This transporter is primarily located in the liver, where it acts as a gatekeeper to pull compounds from the blood into liver cells [1]. It regulates the clearance of essential endogenous substances like bilirubin and bile acids [2]. Additionally, OATP1B1 is responsible for absorbing many widely prescribed medications, particularly cholesterol-lowering statins [1]. When the transporter functions normally, these drugs are efficiently processed and cleared from circulation [1].
Variant Impact: The rs4149056 variant represents a single-letter change from T to C in the SLCO1B1 gene, resulting in a valine-to-alanine amino acid substitution at position 174 of the transporter protein [1]. This specific change, which defines the SLCO1B1*5 star-allele, significantly impairs the transporter's ability to move compounds into the liver [1]. Because the protein cannot efficiently grab molecules from the bloodstream, drugs and certain natural metabolites build up to much higher levels in the body [1]. This reduced transport activity directly increases the risk of drug-induced toxicities, particularly muscle pain and damage from statins [3].
Key Insight: This variant is the single most important genetic predictor of statin-induced muscle pain, and carrying it can increase the risk of severe muscle damage by up to 17-fold depending on the dose and type of statin used.
Location: SLCO1B1. Chromosome 12 · 12p12.1 · 21.2 Mb
Estimated prevalence by population
Global 77.7%; European 70.8%; African 93.8%; East Asian 76.1%; South Asian 90.5%; Americas 75.6%; Ashkenazi 67.7%; Finnish 61.2%; Middle Eastern 62.3%; Amish 86.9%.
Estimated TT genotype frequency.
Global 20.4%; European 26.7%; African 6.1%; East Asian 22.2%; South Asian 9.3%; Americas 22.7%; Ashkenazi 29.1%; Finnish 34.1%; Middle Eastern 33.3%; Amish 12.7%.
Estimated TC genotype frequency.
Global 1.8%; European 2.5%; African 0.1%; East Asian 1.6%; South Asian 0.2%; Americas 1.7%; Ashkenazi 3.1%; Finnish 4.7%; Middle Eastern 4.4%; Amish 0.5%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Pharmacogenomics
Adverse Drug Reactions
Statin Muscle Pain. Evidence: 7/10. Source: PMID 18650507. Typical Risk.
Immunosuppressant & Biologic Response
Methotrexate Toxicity. Evidence: 8/10. Source: PMID 23233662. Typical Risk.
Organ Systems
Liver Function & Disease
Bilirubin Levels. Evidence: 9/10. Source: PMID 19414484. Typical.
Cardiovascular & Metabolic
Gout & Uric Acid
Gout. Evidence: 8/10. Source: PMID 39406924. Slightly Increased.
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Typical.
Showing effects for C/C genotype
Statin Muscle Pain. Evidence: 7/10. Source: PMID 18650507. ~17x Increased Risk.
Methotrexate Toxicity. Evidence: 8/10. Source: PMID 23233662. High Risk.
Bilirubin Levels. Evidence: 9/10. Source: PMID 19414484. Elevated.
Gout. Evidence: 8/10. Source: PMID 39406924. Lower Risk.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Elevated.
Showing effects for T/C genotype
Statin Muscle Pain. Evidence: 7/10. Source: PMID 18650507. ~5x Increased Risk.
Methotrexate Toxicity. Evidence: 8/10. Source: PMID 23233662. Increased Risk.
Bilirubin Levels. Evidence: 9/10. Source: PMID 19414484. Slightly Elevated.
Gout. Evidence: 8/10. Source: PMID 39406924. Typical.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Slightly Elevated.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Carrying two copies of the common T allele results in fully functional OATP1B1 transporter proteins in the liver [1]. This allows cholesterol-lowering statins, such as simvastatin and atorvastatin, to be efficiently absorbed and metabolized [1]. Consequently, drug levels in the bloodstream remain within a safe, therapeutic range, minimizing the risk of muscle toxicity or rhabdomyolysis [2]. While statin tolerance is excellent, this genotype is associated with slightly higher urate levels and a minor increase in gout risk compared to carriers of the C allele [3]. Bilirubin clearance is also highly efficient, maintaining typical levels in the blood [4]. Overall, standard dosing guidelines for statins and other transported drugs apply normally [1].
Normal statin metabolism; Typical risk of muscle side effects; Standard drug clearance rates.
Sample genotype: CC (Homozygous)
Carrying two copies of the C allele results in a severe loss of OATP1B1 transporter activity in the liver [1]. This impairment prevents the efficient uptake of several statins, causing them to accumulate in the bloodstream at highly elevated concentrations [1]. For individuals taking high-dose simvastatin, this genotype is linked to an approximate 17-fold increase in the risk of developing myopathy or severe muscle breakdown [2]. Slower clearance of the chemotherapy drug methotrexate also significantly raises the risk of severe toxicities, including kidney and liver damage [3]. Additionally, the reduced transport of endogenous compounds leads to noticeably higher circulating bilirubin levels [4]. Clinical guidelines strongly recommend avoiding simvastatin and choosing alternative cholesterol-lowering therapies or adjusted doses for individuals with this genetic profile [1].
Severely reduced statin clearance; Up to 17-fold higher risk of muscle toxicity; Significantly slower methotrexate processing.
Sample genotype: TC (Heterozygous)
Carrying one copy of the C allele, also known as the SLCO1B1*5 variant, leads to a moderate reduction in OATP1B1 transporter function [1]. When taking certain cholesterol-lowering statins, particularly simvastatin, the drug cannot enter liver cells efficiently and accumulates in the bloodstream [2]. This elevated systemic exposure increases the risk of statin-induced myopathy, or muscle damage, by approximately five-fold [2]. Other medications, such as the chemotherapy drug methotrexate, are also cleared more slowly, which can increase the risk of side effects like liver or blood toxicity [3]. Conversely, this slower transport slightly elevates circulating bilirubin levels, which is generally harmless but can mimic mild liver clearance issues [4]. Because of these altered pharmacokinetics, alternative statins or lower doses are often recommended by clinical guidelines [1].
Slower clearance of certain statins; Higher risk of statin-induced muscle pain; Altered processing of methotrexate.
Variants with shared genetic architecture
rs11045819 · SLCO1B1 Gene · Chr 12 · Statin Response
rs4149081 · SLCO1B1 Gene · Chr 12 · Statin Response
rs11045879 · SLCO1B1 Gene · Chr 12 · Chemotherapy Toxicity Risk
Genome-wide association meta-analysis for total serum bilirubin levels.
SLCO1B1 variants and statin-induced myopathy--a genomewide study.
A genome-wide association analysis reveals new pathogenic pathways in gout.
Content updated August 2026.
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