What you carry at this position in your DNA and what research says about it.
Gallstone Risk: 6/10 evidence, 17 publications.
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Sample genotype (not yours): A/A
Typical Gallstone Risk and Normal Bilirubin Clearance
Typical enzyme activity supports standard clearance of bilirubin and certain medications. This genotype is associated with a lower risk of gallstones compared to carrying the G allele.
What this genotype means: Typical risk of gallstones; Standard metabolism of valproic acid; Increased risk of irinotecan toxicity.
Sample genotype (not yours): A/G
Increased Gallstone Risk and Faster Drug Metabolism
Carrying one copy of the G allele is associated with elevated bilirubin levels and a higher risk of gallstones. It also leads to faster metabolism of certain medications like valproic acid.
What this genotype means: Increased risk of gallstones; Faster metabolism of valproic acid; Increased risk of irinotecan toxicity.
Sample genotype (not yours): G/G
Highest Gallstone Risk and Accelerated Drug Metabolism
Two copies of the G allele significantly increase bilirubin levels and the risk of gallstones. This genotype also accelerates the metabolism of valproic acid while reducing irinotecan toxicity risk.
What this genotype means: Highest risk of gallstones; Rapid metabolism of valproic acid; Reduced risk of irinotecan toxicity.
Gene function and biological role
Gene Function: The UGT1A6 gene encodes UDP-glucuronosyltransferase 1-6, a major phase II drug-metabolizing enzyme [1]. It plays a critical role in the detoxification and clearance of many therapeutic drugs, including acetaminophen, aspirin, and valproic acid [2] [3]. The enzyme is also involved in the metabolism of endogenous compounds such as estrogens and thyroid hormones [4]. It is part of the UGT1A gene complex on chromosome 2, which produces multiple enzyme isoforms through alternative splicing [4].
Variant Impact: The rs2070959 variant is a missense mutation in the UGT1A6 gene that results in a threonine-to-alanine amino acid substitution at position 181 of the protein, commonly designated as the UGT1A6*2 allele [5]. This amino acid change, often in tight linkage with other coding variants, alters the enzyme's metabolic activity toward various substrates [5] [1]. It is significantly associated with variation in serum bilirubin levels and the risk of developing gallstones [6] [7]. Additionally, this genetic variation influences how the body processes medications like valproic acid and irinotecan [8] [9].
Key Insight: The G allele of this variant is associated with a nearly five-fold increase in the risk of requiring gallbladder removal due to gallstones, driven by elevated bilirubin levels.
Location: UGT1A6. Chromosome 2 · 2q37.1 · 233.7 Mb
Estimated prevalence by population
Global 49.4%; European 46.0%; African 57.2%; East Asian 63.7%; South Asian 35.9%; Americas 59.3%; Ashkenazi 36.3%; Finnish 30.6%; Middle Eastern 42.7%; Amish 29.2%.
Estimated AA genotype frequency.
Global 41.2%; European 43.6%; African 36.9%; East Asian 32.2%; South Asian 48.0%; Americas 35.4%; Ashkenazi 47.9%; Finnish 49.4%; Middle Eastern 45.3%; Amish 49.7%.
Estimated AG genotype frequency.
Global 9.4%; European 10.3%; African 5.9%; East Asian 4.1%; South Asian 16.0%; Americas 5.3%; Ashkenazi 15.8%; Finnish 19.9%; Middle Eastern 12.0%; Amish 21.1%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Organ Systems
Digestive & Gut Disorders
Gallstones. Evidence: 6/10. Source: PMID 30504769. Typical Risk.
Liver Function & Disease
Bilirubin Levels. Evidence: 8/10. Source: PMID 30621171. Typical Levels.
Pharmacogenomics
Antiepileptic & Mood-Stabilizer Response
Valproic Acid Response. Evidence: 5/10. Source: PMID 21806385. Slower Metabolism.
Chemotherapy Response
Irinotecan Toxicity. Evidence: 5/10. Source: PMID 23386248. Increased Risk.
Cancer & Oncology
Gynecological Cancers
Endometrial Cancer. Evidence: 3/10. Source: PMID 18349273. Typical Risk.
Showing effects for A/G genotype
Gallstones. Evidence: 6/10. Source: PMID 30504769. Increased Risk.
Bilirubin Levels. Evidence: 8/10. Source: PMID 30621171. Slightly Higher.
Valproic Acid Response. Evidence: 5/10. Source: PMID 21806385. Faster Metabolism.
Showing effects for G/G genotype
Gallstones. Evidence: 6/10. Source: PMID 30504769. Highest Risk.
Bilirubin Levels. Evidence: 8/10. Source: PMID 30621171. Higher Levels.
Irinotecan Toxicity. Evidence: 5/10. Source: PMID 23386248. Typical Risk.
Endometrial Cancer. Evidence: 3/10. Source: PMID 18349273. Lower Risk.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Typical enzyme activity is maintained with two copies of the common A allele, supporting standard metabolic clearance [1]. Bilirubin levels are typically kept within a normal range because the enzyme efficiently processes this heme byproduct [2]. The risk of developing gallstones or requiring gallbladder removal is significantly lower compared to individuals carrying the G variant [3]. When taking medications like valproic acid, metabolism is slower, which often means standard dosing is effective [4]. However, there is an increased risk of toxicity when treated with the chemotherapy drug irinotecan [5]. Standard clinical monitoring is typically sufficient for managing these risks.
Typical risk of gallstones; Standard metabolism of valproic acid; Increased risk of irinotecan toxicity.
Sample genotype: AG (Heterozygous)
Altered enzyme function occurs when carrying one copy of the G allele, which can affect the clearance of both endogenous compounds and drugs [1]. Bilirubin clearance is slightly reduced, leading to higher circulating levels of this pigment in the blood [2]. This elevation in bilirubin is linked to an increased risk of developing gallstones and a higher likelihood of undergoing gallbladder surgery [3]. Metabolism of the anti-seizure medication valproic acid is accelerated, so the drug reaches lower levels and its effect is correspondingly weaker [4]. There is also an increased risk of experiencing tremors as a side effect of valproic acid therapy [5]. Additionally, this genotype is associated with an increased risk of toxicity from the chemotherapy drug irinotecan [6].
Increased risk of gallstones; Faster metabolism of valproic acid; Increased risk of irinotecan toxicity.
Sample genotype: GG (Homozygous)
Significantly altered glucuronidation capacity is present in individuals with two copies of the G allele [1]. Bilirubin levels are elevated due to reduced clearance, which strongly predisposes to the formation of pigment gallstones [2] [3]. The risk of requiring gallbladder removal is substantially higher than in those with the typical genotype [3]. Valproic acid is metabolized rapidly, often necessitating higher clinical doses to maintain seizure control [4]. This rapid metabolism is also associated with a higher likelihood of developing drug-induced tremors [5]. Conversely, this genotype is linked to a lower risk of severe toxicity and neutropenia when undergoing irinotecan chemotherapy [6]. Women with this genotype may also have a reduced risk of endometrial cancer [7].
Highest risk of gallstones; Rapid metabolism of valproic acid; Reduced risk of irinotecan toxicity; Lower risk of endometrial cancer.
Variants with shared genetic architecture
rs6759892 · UGT1A6 Gene · Chr 2 · Drug and Toxin Metabolism
rs17863783 · UGT1A6 Gene · Chr 2 · Bladder Cancer Risk
rs1105879 · UGT1A6 Gene · Chr 2 · Colorectal Cancer Risk
Association of genetic variants in six candidate genes with valproic acid therapy optimization.
Pharmacogenomics in aspirin intolerance.
Genome-wide association meta-analysis yields 20 loci associated with gallstone disease.
Content updated August 2026.
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