What you carry at this position in your DNA and what research says about it.
Drug Metabolism: 3/10 evidence, 49 publications.
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Sample genotype (not yours): G/G
Typical Drug Metabolism Speed
Two copies of the standard allele result in normal NAT2 enzyme activity. This allows your body to clear medications and environmental toxins at a typical, rapid pace.
What this genotype means: Typical medication clearance; Lower risk of drug-induced liver damage; Baseline risk of age-related hearing loss.
Sample genotype (not yours): A/A
Significantly Slower Drug Metabolism
Carrying two copies of the variant allele significantly reduces your NAT2 enzyme activity, classifying you as a slow acetylator. This notably increases your risk of toxicity and liver damage from specific medications.
What this genotype means: Significantly slower drug clearance; High risk of liver toxicity from TB medications; Increased risk of age-related hearing loss.
Sample genotype (not yours): G/A
Moderately Slower Drug Metabolism
Carrying one copy of the variant allele moderately reduces your NAT2 enzyme activity. This intermediate acetylator status can increase your risk of side effects from certain medications.
What this genotype means: Moderately slower drug clearance; Increased risk of liver toxicity from TB drugs; Slightly higher risk of age-related hearing loss.
Gene function and biological role
Gene Function: The NAT2 gene encodes N-acetyltransferase 2, a critical liver enzyme involved in Phase II detoxification. This enzyme is responsible for metabolizing arylamines, hydrazines, and various therapeutic drugs through a process called acetylation. Genetic variations in this gene divide individuals into rapid, intermediate, and slow acetylators, which directly influences how quickly the body clears certain substances. Slow acetylators tend to accumulate drugs in their system, increasing the risk of toxicity, while rapid acetylators may clear drugs too quickly, reducing treatment efficacy.
Variant Impact: The rs1799930 variant, also known as G590A or NAT2*6A, is a missense mutation that changes the amino acid arginine to glutamine at position 197 of the NAT2 enzyme. This specific structural change reduces the stability and functional activity of the enzyme. Inheriting this variant allele contributes to a slow acetylator phenotype, slowing down the breakdown of various medications and environmental toxins. Consequently, carriers of this variant are more susceptible to adverse drug reactions and chemical-induced cellular stress.
Key Insight: This variant determines how safely your liver processes common medications, and carrying it can significantly increase the risk of liver damage from standard tuberculosis therapies.
Location: NAT2. Chromosome 8 · 8p22 · 18.4 Mb
Estimated prevalence by population
Global 53.0%; European 50.1%; African 55.0%; East Asian 55.2%; South Asian 40.5%; Americas 62.9%; Ashkenazi 40.8%; Finnish 58.7%; Middle Eastern 52.2%; Amish 41.8%.
Estimated GG genotype frequency.
Global 39.4%; European 41.4%; African 38.3%; East Asian 38.2%; South Asian 46.3%; Americas 32.8%; Ashkenazi 46.2%; Finnish 35.9%; Middle Eastern 40.1%; Amish 45.7%.
Estimated GA genotype frequency.
Global 7.6%; European 8.5%; African 6.7%; East Asian 6.6%; South Asian 13.2%; Americas 4.3%; Ashkenazi 13.1%; Finnish 5.5%; Middle Eastern 7.7%; Amish 12.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Drug Metabolism Speed. Evidence: 3/10. Source: PMID 22092036. Typical Speed.
Antimicrobial & Antiviral Response
Antituberculosis Drug Toxicity. Evidence: 6/10. Source: PMID 22506592. Typical Risk.
Co-trimoxazole Sensitivity. Evidence: 5/10. Source: PMID 9923584. Typical Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Typical Risk.
Organ Systems
Hearing & Balance
Age-Related Hearing Loss. Evidence: 3/10. Source: PMID 17513527. Typical Risk.
Showing effects for A/A genotype
Drug Metabolism Speed. Evidence: 3/10. Source: PMID 22092036. Significantly Slower.
Antituberculosis Drug Toxicity. Evidence: 6/10. Source: PMID 22506592. High Risk.
Co-trimoxazole Sensitivity. Evidence: 5/10. Source: PMID 9923584. Increased Risk.
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Increased Risk.
Age-Related Hearing Loss. Evidence: 3/10. Source: PMID 17513527. Increased Risk.
Showing effects for G/A genotype
Drug Metabolism Speed. Evidence: 3/10. Source: PMID 22092036. Moderately Slower.
Antituberculosis Drug Toxicity. Evidence: 6/10. Source: PMID 22506592. Increased Risk.
Age-Related Hearing Loss. Evidence: 3/10. Source: PMID 17513527. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Having the G/G genotype means you possess normal N-acetyltransferase 2 enzyme activity, which is classified as a rapid acetylator status. This genotype is associated with the typical, efficient clearance of common medications like isoniazid, rifampin, and other tuberculosis treatments. Because your liver processes these compounds at a standard rate, you have a lower risk of drug-induced liver damage compared to carriers of the slow-acetylating variant allele. However, rapid clearance can occasionally mean certain medications are processed too quickly, potentially reducing their therapeutic effectiveness. You also maintain a typical, baseline risk for age-related hearing loss.
Typical medication clearance; Lower risk of drug-induced liver damage; Baseline risk of age-related hearing loss.
Sample genotype: AA (Homozygous)
Having the A/A genotype leads to a slow acetylator phenotype due to a significant reduction in NAT2 enzyme activity. This slow clearance rate is strongly linked to an increased risk of severe liver damage and hepatitis when undergoing standard tuberculosis treatments with isoniazid, rifampin, or pyrazinamide. It also predisposes you to higher rates of toxicity from other drugs, including phenytoin and co-trimoxazole. Furthermore, studies have associated this genotype with a higher susceptibility to age-related hearing loss, possibly due to reduced detoxification of oxidative stressors in the inner ear.
Significantly slower drug clearance; High risk of liver toxicity from TB medications; Increased risk of age-related hearing loss.
Sample genotype: GA (Heterozygous)
Carrying the G/A genotype typically results in an intermediate acetylator status, meaning your NAT2 enzyme processes substances at a moderately reduced speed. When taking medications like isoniazid, rifampin, or other anti-tuberculosis drugs, you have a slightly elevated risk of drug-induced liver toxicity or hepatitis. Your body may also clear other drugs, such as the seizure medication phenytoin or the antibiotic co-trimoxazole, more slowly, increasing the likelihood of side effects. Additionally, some research suggests a potential, slight increase in susceptibility to age-related hearing loss.
Moderately slower drug clearance; Increased risk of liver toxicity from TB drugs; Slightly higher risk of age-related hearing loss.
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
Content updated August 2026.
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