What you carry at this position in your DNA and what research says about it.
Bilirubin and Drug Metabolism: 9/10 evidence, 29 publications.
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Sample genotype (not yours): G/G
Typical Bilirubin Levels and Normal Drug Metabolism
Two copies of the normal gene version mean typical enzyme activity. Bilirubin is processed efficiently, and there is no elevated risk of toxicity from related medications.
What this genotype means: Typical bilirubin clearance; Normal processing of irinotecan and cisplatin; Low risk of Gilbert's syndrome.
Sample genotype (not yours): A/A
Elevated Bilirubin Levels and High Drug Sensitivity
Two copies of the decreased-function allele significantly reduce enzyme activity. This is a primary cause of Gilbert's syndrome and greatly increases the risk of severe side effects from specific medications.
What this genotype means: Significantly reduced enzyme activity; High likelihood of Gilbert's syndrome; High risk of severe chemotherapy toxicity.
Sample genotype (not yours): G/A
Slightly Elevated Bilirubin and Increased Drug Sensitivity
Carrying one copy of the decreased-function allele leads to moderately reduced enzyme activity. This can result in slightly higher bilirubin levels and a higher risk of side effects from certain medications.
What this genotype means: Moderately reduced enzyme activity; Slightly elevated bilirubin levels; Increased risk of chemotherapy side effects.
Gene function and biological role
Gene Function: The UGT1A1 gene encodes UDP-glucuronosyltransferase 1-1, an essential enzyme responsible for glucuronidation, a key phase II detoxification process [1]. This enzyme converts lipophilic substances, such as bilirubin and various medications, into water-soluble forms that the body can easily excrete [1] [2]. Proper function of this pathway prevents the toxic accumulation of unconjugated bilirubin in the bloodstream [2]. It also plays a critical role in clearing chemotherapy drugs like irinotecan and other therapeutic agents [3]. Reduced activity of this gene is a primary cause of hereditary hyperbilirubinemia conditions like Gilbert's syndrome [1] [4].
Variant Impact: A single-nucleotide change in exon 1 of the UGT1A1 gene substitutes the amino acid glycine with arginine at position 71 (G71R) [1]. This specific change defines the well-known UGT1A1*6 decreased-function allele [5]. The structural alteration reduces the enzyme's maximum velocity, cutting its overall clearance capacity for bilirubin glucuronidation by approximately half [1]. Consequently, individuals carrying this variant exhibit slower clearance of bilirubin and specific medications [6]. This variant is particularly prevalent in East Asian populations, where it serves as a major genetic determinant of bilirubin levels and drug-induced toxicities [6] [7].
Key Insight: Although the UGT1A1*6 variant is highly common in East Asian populations, it is virtually absent in people of European and African descent.
Location: UGT1A1. Chromosome 2 · 2q37.1 · 233.8 Mb
Estimated prevalence by population
Global 97.8%; European 99.8%; African 99.8%; East Asian 71.5%; South Asian 96.0%; Americas 97.7%; Ashkenazi 99.4%; Finnish 90.8%; Middle Eastern 100.0%; Amish 100.0%.
Estimated GG genotype frequency.
Global 2.1%; European 0.2%; African 0.2%; East Asian 26.1%; South Asian 3.9%; Americas 2.3%; Ashkenazi 0.6%; Finnish 9.0%; Middle Eastern 0.0%; Amish 0.0%.
Estimated GA genotype frequency.
Global 0.1%; European < 0.1%; African < 0.1%; East Asian 2.4%; South Asian < 0.1%; Americas < 0.1%; Ashkenazi < 0.1%; Finnish 0.2%; Middle Eastern 0.0%; Amish 0.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Organ Systems
Liver Function & Disease
Bilirubin Levels. Evidence: 9/10. Source: PMID 20639394. Typical.
Newborn Jaundice. Evidence: 5/10. Source: PMID 20975617. Typical Risk.
Pharmacogenomics
Chemotherapy Response
Irinotecan Toxicity. Evidence: 8/10. Source: PMID 19299905. Typical Risk.
Cisplatin Toxicity. Evidence: 8/10. Source: PMID 19299905. Typical Risk.
Cardiovascular Drug Response
Carvedilol Metabolism. Evidence: 8/10. Source: PMID 16849011. Normal.
Rare Genetic Disorders
Inherited Metabolic Disorders
Gilbert Syndrome. Evidence: 5/10. Source: PMID 9630669. Typical Risk.
Showing effects for A/A genotype
Bilirubin Levels. Evidence: 9/10. Source: PMID 20639394. Elevated.
Newborn Jaundice. Evidence: 5/10. Source: PMID 20975617. High Risk.
Irinotecan Toxicity. Evidence: 8/10. Source: PMID 19299905. High Risk.
Cisplatin Toxicity. Evidence: 8/10. Source: PMID 19299905. High Risk.
Carvedilol Metabolism. Evidence: 8/10. Source: PMID 16849011. Slower.
Gilbert Syndrome. Evidence: 5/10. Source: PMID 9630669. High Risk.
Showing effects for G/A genotype
Bilirubin Levels. Evidence: 9/10. Source: PMID 20639394. Slightly Elevated.
Newborn Jaundice. Evidence: 5/10. Source: PMID 20975617. Increased Risk.
Irinotecan Toxicity. Evidence: 8/10. Source: PMID 19299905. Increased Risk.
Cisplatin Toxicity. Evidence: 8/10. Source: PMID 19299905. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Possessing two copies of the functional G allele ensures normal activity of the UDP-glucuronosyltransferase enzyme [1]. Bilirubin, a byproduct of red blood cell breakdown, is processed and cleared from the body at a typical rate [1] [2]. This genotype is associated with a low risk of developing Gilbert's syndrome or neonatal jaundice [1] [3]. Additionally, standard doses of medications metabolized by this enzyme, such as the chemotherapy drug irinotecan, are processed normally [4]. This minimizes the risk of severe side effects like neutropenia or severe diarrhea during treatment [4]. Slower metabolism of other drugs like carvedilol or cisplatin is also not expected with this baseline genotype [5]. Overall, this represents the most common and optimal genetic profile for bilirubin clearance and drug safety.
Typical bilirubin clearance; Normal processing of irinotecan and cisplatin; Low risk of Gilbert's syndrome.
Sample genotype: AA (Homozygous)
Inheriting two copies of the UGT1A1*6 allele leads to a significant reduction in enzyme activity, often by half or more [1]. This genetic profile is strongly associated with Gilbert's syndrome, a benign condition characterized by elevated levels of unconjugated bilirubin in the blood [1] [2]. Newborns with this genotype are at a much higher risk of experiencing prolonged neonatal jaundice [3]. Crucially, this genotype dramatically increases the risk of severe, potentially life-threatening toxicities, such as profound neutropenia and severe diarrhea, when treated with the chemotherapy drug irinotecan [4]. Slower clearance of other drugs, such as cisplatin, carvedilol, and letermovir, is also highly likely [4] [5] [6].
Significantly reduced enzyme activity; High likelihood of Gilbert's syndrome; High risk of severe chemotherapy toxicity.
Sample genotype: GA (Heterozygous)
Possessing one copy of the UGT1A1*6 allele reduces the overall capacity to process bilirubin and clear specific drugs [1]. Bilirubin levels in the blood may be slightly higher than average, though usually remaining below the threshold for clinical Gilbert's syndrome [1] [2]. However, infants carrying this genotype may have an increased risk of developing transient neonatal jaundice [3]. When undergoing chemotherapy with irinotecan or cisplatin, there is a moderately elevated risk of experiencing severe side effects such as neutropenia and diarrhea [4]. Slower metabolism may also affect other medications, including the beta-blocker carvedilol and the antiviral letermovir [5] [6]. Knowing this status can help healthcare providers tailor drug choices and monitor side effects more closely if these medications are prescribed.
Moderately reduced enzyme activity; Slightly elevated bilirubin levels; Increased risk of chemotherapy side effects.
Variants with shared genetic architecture
rs6742078 · UGT1A1 Gene · Chr 2 · Gallstone Risk
rs887829 · UGT1A1 Gene · Chr 2 · Bilirubin and Heart Health
rs10929302 · UGT1A1 Gene · Chr 2 · Drug and Bilirubin Clearance
UGT1A1 sequence variants associated with risk of adult hyperbilirubinemia: a quantitative analysis.
Genome-wide association of serum bilirubin levels in Korean population.
211 G to a variation of UDP-glucuronosyl transferase 1A1 gene and neonatal breastfeeding jaundice.
Content updated August 2026.
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