What you carry at this position in your DNA and what research says about it.
Drug Clearance and Toxicity: 6/10 evidence, 33 publications.
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Sample genotype (not yours): G/G
Typical Drug Clearance and Lower Toxicity Risk
Normal enzyme activity allows for typical processing of medications and environmental toxins. This reduces the risk of liver damage and other side effects from specific drugs.
What this genotype means: Typical clearance of medications; Lower risk of drug-induced liver injury; Typical sensitivity to environmental toxins.
Sample genotype (not yours): A/A
Slow Drug Clearance and High Toxicity Risk
Significantly reduced enzyme activity leads to very slow processing of medications and toxins. This highly elevates the risk of severe drug side effects and liver damage.
What this genotype means: Very slow clearance of specific medications; High risk of drug-induced liver damage; Increased sensitivity to environmental toxins.
Sample genotype (not yours): G/A
Intermediate Drug Clearance and Increased Toxicity Risk
Reduced enzyme activity slows down the processing of certain medications and toxins. This moderately increases the risk of side effects and liver irritation.
What this genotype means: Slower clearance of specific medications; Increased risk of drug-induced liver irritation; Moderate sensitivity to environmental chemicals.
Gene function and biological role
Gene Function: The NAT2 gene encodes N-acetyltransferase 2, an enzyme primarily active in the liver that plays a critical role in metabolizing foreign substances [1]. It is responsible for the detoxification of various environmental toxins, carcinogens, and common medications [2]. This enzyme works by transferring an acetyl group to arylamine and hydrazine compounds, a process known as acetylation [1]. Genetic variations in this gene divide the population into rapid, intermediate, and slow acetylators [3]. Slow acetylators clear certain drugs much more slowly, which can lead to higher drug concentrations and an increased risk of toxicity [2].
Variant Impact: The rs1799931 variant represents a single nucleotide change from guanine to adenine in the NAT2 gene, resulting in an amino acid substitution of glycine with glutamate at position 286 of the protein [4]. This specific structural change alters the stability and activity of the N-acetyltransferase 2 enzyme, significantly reducing its capacity to process compounds [4]. Known as the signature marker for the NAT2*7 allele family, this variant is one of the primary genetic determinants of the slow acetylator phenotype [5]. It is particularly prevalent in East Asian populations, where it serves as a key marker for predicting drug clearance rates [3].
Key Insight: This variant is a major determinant of whether you are a slow or rapid drug metabolizer, which directly impacts how your liver handles common antibiotics and tuberculosis medications.
Location: NAT2. Chromosome 8 · 8p22 · 18.4 Mb
Origin Story: The distribution of NAT2 slow-acetylator variants in human populations is thought to reflect ancient dietary transitions, where the shift from foraging to farming altered exposure to natural toxins and dietary carcinogens.
Estimated prevalence by population
Global 92.0%; European 94.9%; African 93.5%; East Asian 72.1%; South Asian 85.7%; Americas 81.7%; Ashkenazi 95.9%; Finnish 93.3%; Middle Eastern 90.1%; Amish 99.6%.
Estimated GG genotype frequency.
Global 7.7%; European 5.0%; African 6.4%; East Asian 25.6%; South Asian 13.7%; Americas 17.4%; Ashkenazi 4.0%; Finnish 6.6%; Middle Eastern 9.7%; Amish 0.4%.
Estimated GA genotype frequency.
Global 0.3%; European 0.1%; African 0.1%; East Asian 2.3%; South Asian 0.5%; Americas 0.9%; Ashkenazi < 0.1%; Finnish 0.1%; Middle Eastern 0.3%; Amish < 0.1%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Antimicrobial & Antiviral Response
Antituberculosis Drug Toxicity. Evidence: 6/10. Source: PMID 20392357. Typical Risk.
Antibiotic Side Effects. Evidence: 5/10. Source: PMID 9923584. Typical Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Typical Risk.
Cancer & Oncology
Urologic Cancers
Bladder Cancer. Evidence: 3/10. Source: PMID 16112301. Typical Risk.
Showing effects for A/A genotype
Antituberculosis Drug Toxicity. Evidence: 6/10. Source: PMID 20392357. High Risk.
Antibiotic Side Effects. Evidence: 5/10. Source: PMID 9923584. High Risk.
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. High Risk.
Bladder Cancer. Evidence: 3/10. Source: PMID 16112301. High Risk.
Showing effects for G/A genotype
Antituberculosis Drug Toxicity. Evidence: 6/10. Source: PMID 20392357. Increased Risk.
Antibiotic Side Effects. Evidence: 5/10. Source: PMID 9923584. Increased Risk.
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Increased Risk.
Bladder Cancer. Evidence: 3/10. Source: PMID 16112301. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Normal N-acetyltransferase 2 enzyme function ensures that medications like isoniazid are metabolized at a typical rate [1]. This rapid clearance prevents the accumulation of toxic drug byproducts, significantly lowering the risk of drug-induced liver injury during tuberculosis treatment [2]. Additionally, typical enzyme activity helps detoxify environmental chemicals, which is associated with a lower risk of bladder cancer compared to slow acetylators [3]. Standard dosing guidelines for medications metabolized by this pathway are generally optimized for this typical metabolizer profile [4].
Typical clearance of medications; Lower risk of drug-induced liver injury; Typical sensitivity to environmental toxins.
Sample genotype: AA (Homozygous)
Having two copies of the variant allele results in a slow acetylator phenotype with highly compromised enzyme activity [1]. Medications like isoniazid and other tuberculosis therapies clear very slowly, leading to a high risk of drug-induced hepatotoxicity [2]. The clearance of other drugs, including the antiseizure medication phenytoin and certain antibiotics, is also severely delayed, which can trigger toxic side effects [3]. Furthermore, slow acetylation impairs the detoxification of environmental chemicals, which has been linked to an increased susceptibility to bladder cancer [4].
Very slow clearance of specific medications; High risk of drug-induced liver damage; Increased sensitivity to environmental toxins.
Sample genotype: GA (Heterozygous)
Carrying one copy of the slow-acetylator variant reduces the overall processing speed of the N-acetyltransferase 2 enzyme [1]. This intermediate metabolism rate can lead to a gradual buildup of drugs such as isoniazid, increasing the risk of liver damage during treatment [2]. Similarly, the clearance of other medications like phenytoin or sulfamethoxazole may be delayed, elevating the likelihood of experiencing adverse drug reactions [3]. While intermediate acetylators often tolerate standard doses, they remain more sensitive to chemical exposures and drug toxicities than rapid acetylators [4].
Slower clearance of specific medications; Increased risk of drug-induced liver irritation; Moderate sensitivity to environmental chemicals.
Variants with shared genetic architecture
rs1495741 · NAT2 Gene · Chr 8 · Drug and Toxin Metabolism
rs1041983 · NAT2 Gene · Chr 8 · Drug Metabolism Speed
rs1495743 · NAT2 Gene · Chr 8 · Cholesterol Levels
Structure/function evaluations of single nucleotide polymorphisms in human N-acetyltransferase 2.
Content updated August 2026.
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