What you carry at this position in your DNA and what research says about it.
Hepatitis B Resistance: 8/10 evidence, 8 publications.
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Sample genotype (not yours): G/G
Typical Hepatitis B Susceptibility and Normal Gallstone Risk
Liver cells possess fully functional transport proteins that allow normal bile acid uptake. This typical function also leaves the liver susceptible to hepatitis B virus entry.
What this genotype means: Typical risk of hepatitis B infection; Low baseline risk of gallstones; Standard cholesterol levels.
Sample genotype (not yours): A/A
Strong Resistance to Hepatitis B but Higher Gallstone Risk
Two copies of the variant almost completely block hepatitis B virus entry into liver cells, providing powerful resistance to infection. However, the severe reduction in bile acid transport elevates blood bile acids and gallstone risk.
What this genotype means: High resistance to hepatitis B infection; Significantly increased risk of gallstones; Markedly lower LDL cholesterol.
Sample genotype (not yours): G/A
Reduced Hepatitis B Risk with Slightly Higher Gallstone Susceptibility
A single copy of the variant reduces the number of functional viral entry receptors on liver cells, offering moderate protection against hepatitis B. This change slightly increases blood bile acids and the risk of gallstones.
What this genotype means: Lower risk of chronic hepatitis B infection; Slightly increased risk of gallstones; Slightly lower LDL cholesterol.
Gene function and biological role
Gene Function: The SLC10A1 gene encodes the sodium/taurocholate cotransporting polypeptide, a crucial protein found on the surface of liver cells. This transporter is primarily responsible for absorbing bile acids from the bloodstream back into the liver, maintaining healthy cholesterol and bile acid balance. In addition to its metabolic role, this protein acts as the essential entry receptor that the hepatitis B virus uses to infect liver cells. Variations in this gene can alter both bile acid transport efficiency and viral susceptibility.
Variant Impact: The rs2296651 variant represents a missense mutation in the SLC10A1 gene, resulting in the substitution of phenylalanine for serine at position 267 of the protein. This specific change, often called S267F, significantly impairs the transporter's ability to bind and move bile acids into hepatocytes. Because the altered protein cannot properly bind the hepatitis B virus, this molecular change also blocks viral entry into liver cells. The variant is highly prevalent in East Asian populations but virtually absent in European and African ancestries.
Key Insight: The same genetic change that protects against hepatitis B virus infection also lowers blood cholesterol levels but increases the risk of developing gallstones.
Location: SLC10A1. Chromosome 14 · 14q24.1 · 69.8 Mb
Origin Story: The S267F variant is thought to have risen in frequency in East Asian populations due to historical selective pressure from hepatitis B epidemics, trading off metabolic efficiency for viral resistance.
Estimated prevalence by population
Global 99.4%; European 100.0%; African 99.7%; East Asian 86.5%; South Asian 100.0%; Americas 99.8%; Ashkenazi 100.0%; Finnish 100.0%; Middle Eastern 100.0%; Amish 100.0%.
Estimated GG genotype frequency.
Global 0.5%; European 0.0%; African 0.3%; East Asian 13.1%; South Asian 0.0%; Americas 0.2%; Ashkenazi 0.0%; Finnish 0.0%; Middle Eastern 0.0%; Amish 0.0%.
Estimated GA genotype frequency.
Global < 0.1%; European 0.0%; African < 0.1%; East Asian 0.5%; South Asian 0.0%; Americas < 0.1%; Ashkenazi 0.0%; Finnish 0.0%; Middle Eastern 0.0%; Amish 0.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Immunity & Inflammation
Infection Susceptibility & Resistance
Hepatitis B Resistance. Evidence: 8/10. Source: PMID 39547589. Typical Risk.
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 9/10. Source: PMID 40436827. Typical Levels.
Total Cholesterol. Evidence: 9/10. Source: PMID 38116116. Typical Levels.
Organ Systems
Digestive & Gut Disorders
Gallstones. Evidence: 6/10. Source: PMID 38116116. Typical Risk.
Liver Function & Disease
Blood Bile Acids. Evidence: 6/10. Source: PMID 38297123. Typical Levels.
Pharmacogenomics
Lipid-Lowering Drug Response
Pravastatin Clearance. Evidence: 5/10. Source: PMID 26744986. Typical Clearance.
Showing effects for A/A genotype
Hepatitis B Resistance. Evidence: 8/10. Source: PMID 39547589. Strong Resistance.
LDL Cholesterol. Evidence: 9/10. Source: PMID 40436827. Markedly Lowered.
Total Cholesterol. Evidence: 9/10. Source: PMID 38116116. Markedly Lowered.
Gallstones. Evidence: 6/10. Source: PMID 38116116. Increased Risk.
Blood Bile Acids. Evidence: 6/10. Source: PMID 38297123. Markedly Elevated.
Pravastatin Clearance. Evidence: 5/10. Source: PMID 26744986. Faster Clearance.
Showing effects for G/A genotype
Hepatitis B Resistance. Evidence: 8/10. Source: PMID 39547589. Increased Resistance.
LDL Cholesterol. Evidence: 9/10. Source: PMID 40436827. Slightly Lowered.
Total Cholesterol. Evidence: 9/10. Source: PMID 38116116. Slightly Lowered.
Gallstones. Evidence: 6/10. Source: PMID 38116116. Slightly Increased.
Blood Bile Acids. Evidence: 6/10. Source: PMID 38297123. Slightly Elevated.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Standard liver function is maintained with the G/G genotype, ensuring that cells express fully functional transport proteins that efficiently clear bile acids from the bloodstream. While this maintains low blood bile acid levels, it also provides an open gateway for the hepatitis B virus to enter and infect hepatocytes. Consequently, this genotype is associated with typical susceptibility to chronic hepatitis B infection and its long-term complications, such as liver cirrhosis. On the positive side, normal bile acid transport keeps the risk of developing gallstones low compared to variant carriers. Cholesterol levels, including LDL and total cholesterol, tend to be at typical baseline levels. Pravastatin clearance also proceeds at a standard rate.
Typical risk of hepatitis B infection; Low baseline risk of gallstones; Standard cholesterol levels.
Sample genotype: AA (Homozygous)
Inheriting two copies of the A allele leads to a near-complete loss of functional transport proteins on the surface of liver cells. Because the hepatitis B virus cannot bind to these altered proteins, this genotype provides robust, near-total resistance to chronic hepatitis B infection. However, the lack of active transport causes bile acids to accumulate in the bloodstream, a condition known as hypercholanemia. This accumulation is associated with a significantly higher risk of developing gallstones. On the metabolic side, this genotype is linked to markedly lower levels of LDL and total cholesterol. It also leads to faster clearance of pravastatin, which can reduce the therapeutic efficacy of this statin.
High resistance to hepatitis B infection; Significantly increased risk of gallstones; Markedly lower LDL cholesterol.
Sample genotype: GA (Heterozygous)
Presence of a single A allele results in a mixture of normal and altered transport proteins on liver cells. The altered proteins fail to bind the hepatitis B virus, which significantly lowers the risk of contracting chronic hepatitis B. This partial block also leads to slightly higher levels of circulating bile acids because clearance from the blood is less efficient. Over time, this altered bile balance is linked to a modest increase in the risk of developing gallstones. Conversely, the liver compensates by pulling less cholesterol from the blood, resulting in slightly lower total and LDL cholesterol levels. Pravastatin is cleared from the body slightly faster, which may subtly influence drug exposure.
Lower risk of chronic hepatitis B infection; Slightly increased risk of gallstones; Slightly lower LDL cholesterol.
Variants with shared genetic architecture
rs4240624 · PPP1R3B Gene · Chr 8 · Gallstone and Cholesterol Risk
rs11887534 · ABCG8 Gene · Chr 2 · Gallstone Risk
rs1497406 · EPHA2 Gene · Chr 1 · Liver and Metabolic Health
Content updated August 2026.
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