What you carry at this position in your DNA and what research says about it.
Gout and Uric Acid Risk: 10/10 evidence, 107 publications.
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Sample genotype (not yours): G/G
Typical Gout and Uric Acid Risk
Normal transporter function maintains typical uric acid levels and standard responses to common medications. Gout risk is at the baseline level for the general population.
What this genotype means: Typical uric acid levels; Standard response to rosuvastatin; Baseline risk of gout.
Sample genotype (not yours): G/T
Increased Risk of Gout and Medication Sensitivity
One copy of the variant allele reduces transporter function, leading to higher uric acid levels and an increased risk of gout. It also alters how the body processes several common medications.
What this genotype means: ~1.7x to 1.9x higher gout risk; Elevated blood uric acid levels; Increased sensitivity to rosuvastatin.
Sample genotype (not yours): T/T
Significantly Elevated Gout Risk and High Drug Sensitivity
Two copies of the variant allele severely compromise transporter function, leading to high uric acid levels and a strong predisposition to gout. Medication clearance is significantly slowed.
What this genotype means: Highly elevated gout risk; Significantly higher uric acid levels; Markedly altered response to rosuvastatin and allopurinol.
Gene function and biological role
Gene Function: The ABCG2 gene encodes a major transporter protein known as Breast Cancer Resistance Protein, which is highly expressed in the intestines and kidneys [1]. This transporter plays a crucial role in pumping various compounds out of cells, including uric acid and several common medications [2]. When ABCG2 functions normally, it helps maintain healthy blood uric acid levels by promoting its excretion into the gut and urine [2]. It also acts as a protective barrier, limiting the absorption and tissue accumulation of certain drugs and toxins [1].
Variant Impact: The rs2231142 variant is a missense mutation in the ABCG2 gene that changes the amino acid at position 141 from glutamine to lysine, commonly referred to as the Q141K or C421A variant [3]. This specific change destabilizes the transporter protein, leading to a significant reduction in its expression and transport activity [2]. Because the transporter cannot efficiently export its targets, uric acid builds up in the bloodstream, and certain medications are cleared from the body much more slowly [2]. This single nucleotide change is one of the most significant genetic determinants of uric acid levels and gout risk in human populations [3].
Key Insight: This variant is responsible for an estimated ten percent of all gout cases in people of European descent and acts as a major genetic switch for statin sensitivity.
Location: ABCG2. Chromosome 4 · 4q22.1 · 88.1 Mb
Estimated prevalence by population
Global 82.6%; European 79.4%; African 94.1%; East Asian 47.6%; South Asian 82.0%; Americas 74.3%; Ashkenazi 87.1%; Finnish 86.4%; Middle Eastern 89.4%; Amish 72.6%.
Estimated GG genotype frequency.
Global 16.3%; European 19.5%; African 5.8%; East Asian 42.8%; South Asian 17.1%; Americas 23.8%; Ashkenazi 12.5%; Finnish 13.1%; Middle Eastern 10.3%; Amish 25.2%.
Estimated GT genotype frequency.
Global 1.2%; European 1.2%; African 0.1%; East Asian 9.6%; South Asian 0.9%; Americas 1.9%; Ashkenazi 0.4%; Finnish 0.5%; Middle Eastern 0.3%; Amish 2.2%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Gout & Uric Acid
Gout. Evidence: 10/10. Source: PMID 21983786. Typical Risk.
Uric Acid Levels. Evidence: 10/10. Source: PMID 18834626. Typical Levels.
Allopurinol Response. Evidence: 9/10. Source: PMID 25676789. Normal Response.
Organ Systems
Kidney Function & Disease
Kidney Stones. Evidence: 10/10. Source: PMID 34594039. Typical Risk.
Pharmacogenomics
Lipid-Lowering Drug Response
Rosuvastatin Response. Evidence: 8/10. Source: PMID 19474787. Normal Response.
Showing effects for G/T genotype
Gout. Evidence: 10/10. Source: PMID 21983786. ~1.7x to 1.9x Risk.
Uric Acid Levels. Evidence: 10/10. Source: PMID 18834626. Elevated Levels.
Allopurinol Response. Evidence: 9/10. Source: PMID 25676789. Poorer Response.
Kidney Stones. Evidence: 10/10. Source: PMID 34594039. Slightly Increased.
Rosuvastatin Response. Evidence: 8/10. Source: PMID 19474787. Increased Sensitivity.
Showing effects for T/T genotype
Gout. Evidence: 10/10. Source: PMID 21983786. Highly Elevated Risk.
Uric Acid Levels. Evidence: 10/10. Source: PMID 18834626. Significantly Elevated.
Kidney Stones. Evidence: 10/10. Source: PMID 34594039. Increased Risk.
Rosuvastatin Response. Evidence: 8/10. Source: PMID 19474787. High Sensitivity.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Normal levels of the ABCG2 transporter protein are maintained by carrying two copies of the common G allele [1]. This allows the body to efficiently export uric acid, preventing it from accumulating in the bloodstream and forming painful crystals in the joints [2]. Consequently, this genotype is associated with a typical risk of developing gout and kidney stones [2]. Standard doses of cholesterol-lowering statins like rosuvastatin are processed normally, without an elevated risk of side effects [3]. Similarly, if gout treatment is ever required, first-line medications like allopurinol typically work as expected [4]. Maintaining a balanced diet and staying hydrated further supports healthy kidney function and uric acid clearance. Overall, cardiovascular and metabolic markers related to this transporter remain at baseline levels. No special dietary or medical precautions are typically recommended based on this genetic profile.
Typical uric acid levels; Standard response to rosuvastatin; Baseline risk of gout.
Sample genotype: GT (Heterozygous)
A single copy of the T allele reduces the abundance and activity of the ABCG2 transporter protein [1]. This reduction impairs the body's ability to excrete uric acid, resulting in higher circulating levels in the blood [2]. Studies show this genotype increases the risk of developing gout by approximately 1.7 to 1.9 times [3]. Additionally, the slower clearance of certain drugs can lead to higher blood concentrations of medications like rosuvastatin, increasing both their efficacy and the risk of muscle-related side effects [4]. Gout therapies like allopurinol may also be less effective, so the desired uric acid reduction can be harder to achieve [5]. Managing dietary intake of purine-rich foods, such as red meat and seafood, can help mitigate the elevated uric acid levels. Staying well-hydrated is also beneficial for supporting kidney function and reducing stone risk. Discussing these genetic tendencies with a healthcare provider can help tailor medication choices and dosages safely.
~1.7x to 1.9x higher gout risk; Elevated blood uric acid levels; Increased sensitivity to rosuvastatin.
Sample genotype: TT (Homozygous)
Severe loss of ABCG2 transporter function occurs when carrying two copies of the T allele [1]. Uric acid excretion is heavily compromised, leading to significantly elevated blood uric acid levels and a highly increased risk of gout and kidney stones [2]. This genotype is a well-established genetic cause of hyperuricemia and gouty arthritis [3]. Because the transporter is also responsible for clearing many drugs, individuals with this genotype experience much higher blood levels of medications like rosuvastatin [4]. This high exposure can dramatically increase the drug's cholesterol-lowering effect but also elevates the risk of adverse side effects [4]. Furthermore, standard gout treatments like allopurinol are frequently less effective [5]. Healthcare providers can use this information to select alternative therapies or adjust medication doses to prevent toxicity.
Highly elevated gout risk; Significantly higher uric acid levels; Markedly altered response to rosuvastatin and allopurinol.
Variants with shared genetic architecture
rs4148155 · ABCG2 Gene · Chr 4 · Gout and Kidney Stones
rs2199936 · ABCG2 Gene · Chr 4 · Gout Risk
rs1481012 · ABCG2 Gene · Chr 4 · Gout and Kidney Stones
Identification of a urate transporter, ABCG2, with a common functional polymorphism causing gout.
ABCG2 polymorphism markedly affects the pharmacokinetics of atorvastatin and rosuvastatin.
Identification of low-frequency variants associated with gout and serum uric acid levels.
ABCG2 contributes to the development of gout and hyperuricemia in a genome-wide association study.
Content updated August 2026.
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