What you carry at this position in your DNA and what research says about it.
Drug Metabolism Speed: 8/10 evidence, 27 publications.
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Sample genotype (not yours): C/C
Typical Drug Metabolism and Standard Toxicity Risk
Standard metabolism of medications and foreign compounds is expected. There is no elevated risk of liver damage from common tuberculosis treatments or anti-seizure drugs.
What this genotype means: Standard drug clearance rates; Typical risk of drug-induced liver injury; Efficient caffeine processing.
Sample genotype (not yours): C/T
Intermediate Drug Metabolism and Elevated Toxicity Risk
Moderate clearance of certain medications may lead to a higher risk of side effects. Specific drugs can clear more slowly than average.
What this genotype means: Slower clearance of certain medications; Elevated risk of drug-induced liver injury; Slightly slower caffeine processing.
Sample genotype (not yours): T/T
Slow Drug Metabolism and High Toxicity Risk
Slower clearance of medications significantly increases the risk of drug-induced liver damage and toxicity.
What this genotype means: Slow drug clearance rates; High risk of drug-induced liver injury; Increased sensitivity to caffeine.
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 the detoxification of foreign chemicals and drugs [1]. This enzyme is responsible for N-acetylation, a metabolic pathway that inactivates various hydrazine and arylamine drugs, including those used to treat tuberculosis [2]. It also processes environmental toxins, heterocyclic amines from cooked meats, and caffeine [3]. Genetic variations in this gene divide the population into rapid, intermediate, and slow acetylators, which directly influences how quickly drugs are cleared from the body [4]. Slow acetylators are at a significantly higher risk of experiencing drug toxicities, while rapid acetylators may clear medications too quickly for them to be fully effective [1].
Variant Impact: The rs1041983 variant is a synonymous single nucleotide change in the coding region of the NAT2 gene, often referred to as C282T [5]. Although it does not alter the amino acid sequence of the N-acetyltransferase 2 protein, it serves as a critical marker for predicting the overall acetylator phenotype [6]. The presence of the T allele is strongly linked to the slow-acetylator phenotype, particularly when inherited alongside other specific NAT2 variants [4]. This genetic marker is widely used in simplified genotyping panels to accurately infer a person's drug clearance rate without needing to sequence the entire gene [6].
Key Insight: Although this genetic variant does not change the actual structure of the protein, it is one of the most powerful predictors of how fast your body detoxifies medications.
Location: NAT2. Chromosome 8 · 8p22 · 18.4 Mb
Origin Story: The slow-acetylator phenotype appears to have undergone positive natural selection in western and central Eurasians over the last several thousand years, potentially driven by dietary changes during the transition to agriculture.
Estimated prevalence by population
Global 41.4%; European 46.5%; African 30.3%; East Asian 34.5%; South Asian 31.7%; Americas 46.2%; Ashkenazi 38.2%; Finnish 53.7%; Middle Eastern 45.1%; Amish 41.6%.
Estimated CC genotype frequency.
Global 45.3%; European 43.4%; African 49.5%; East Asian 48.5%; South Asian 49.2%; Americas 43.6%; Ashkenazi 47.2%; Finnish 39.2%; Middle Eastern 44.1%; Amish 45.8%.
Estimated CT genotype frequency.
Global 13.3%; European 10.1%; African 20.2%; East Asian 17.1%; South Asian 19.1%; Americas 10.3%; Ashkenazi 14.6%; Finnish 7.2%; Middle Eastern 10.8%; Amish 12.6%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Antimicrobial & Antiviral Response
Tuberculosis Drug Liver Injury. Evidence: 6/10. Source: PMID 22506592. Typical Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Typical Risk.
Nutrition & Metabolism
Caffeine & Stimulant Metabolism
Caffeine Metabolism. Evidence: 6/10. Source: PMID 36635386. Faster Metabolism.
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 8/10. Source: PMID 36329257. Slightly Higher.
Total Cholesterol. Evidence: 8/10. Source: PMID 36329257. Slightly Higher.
Showing effects for C/T genotype
Tuberculosis Drug Liver Injury. Evidence: 6/10. Source: PMID 22506592. Increased Risk.
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Increased Risk.
Caffeine Metabolism. Evidence: 6/10. Source: PMID 36635386. Intermediate Speed.
Triglycerides. Evidence: 8/10. Source: PMID 36329257. Typical.
Total Cholesterol. Evidence: 8/10. Source: PMID 36329257. Typical.
Showing effects for T/T genotype
Tuberculosis Drug Liver Injury. Evidence: 6/10. Source: PMID 22506592. High Risk.
Caffeine Metabolism. Evidence: 6/10. Source: PMID 36635386. Slower Metabolism.
Triglycerides. Evidence: 8/10. Source: PMID 36329257. Slightly Lower.
Total Cholesterol. Evidence: 8/10. Source: PMID 36329257. Slightly Lower.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Standard enzymatic activity of N-acetyltransferase 2 allows for the normal clearance of many prescription medications [1]. Standard processing of tuberculosis therapies like isoniazid, rifampin, and pyrazinamide minimizes the risk of drug-induced liver injury [2]. Standard clearance rates also apply to phenytoin, an anti-seizure medication that can build up to toxic levels in slow metabolizers [3]. While drug tolerance is typical, metabolic studies show slightly higher levels of caffeine metabolites, suggesting efficient caffeine processing [4]. Large-scale genomic data also link this genotype to slightly higher baseline levels of triglycerides and total cholesterol [5]. These minor lipid variations are common.
Standard drug clearance rates; Typical risk of drug-induced liver injury; Efficient caffeine processing.
Sample genotype: CT (Heterozygous)
Reduced enzymatic activity of N-acetyltransferase 2 characterizes this intermediate metabolizer status [1]. Processing of several common medications occurs at a slower rate, which can lead to drug accumulation [2]. Clinical studies show an increased risk of liver damage when undergoing standard tuberculosis treatment regimens containing isoniazid, rifampin, or pyrazinamide [3]. Similarly, the anti-seizure medication phenytoin may clear more slowly, raising the likelihood of drug toxicity [4]. Caffeine is also processed at a slightly slower rate compared to rapid metabolizers [5]. On the other hand, lipid profiles may show slightly lower triglycerides and total cholesterol compared to the rapid metabolizer genotype [6].
Slower clearance of certain medications; Elevated risk of drug-induced liver injury; Slightly slower caffeine processing.
Sample genotype: TT (Homozygous)
Severely reduced N-acetyltransferase 2 activity leads to a slow-acetylator phenotype [1]. Medications and environmental toxins remain in the bloodstream for longer periods, increasing the risk of adverse reactions [2]. Standard doses of tuberculosis drugs such as isoniazid, rifampin, pyrazinamide, and ethambutol carry a high risk of causing liver injury [3]. Anti-seizure therapies like phenytoin are also highly prone to reaching toxic levels due to delayed clearance [4]. Caffeine metabolism is notably slower, which may increase sensitivity to caffeinated beverages [5]. Interestingly, this slow-metabolizing state is associated with slightly lower levels of triglycerides and total cholesterol [6].
Slow drug clearance rates; High risk of drug-induced liver injury; Increased sensitivity to caffeine.
Variants with shared genetic architecture
rs1495741 · NAT2 Gene · Chr 8 · Drug and Toxin Metabolism
rs1495743 · NAT2 Gene · Chr 8 · Cholesterol Levels
rs4921913 · NAT2 Gene · Chr 8 · Blood Lipid Levels
Structure/function evaluations of single nucleotide polymorphisms in human N-acetyltransferase 2.
Genomic atlas of the plasma metabolome prioritizes metabolites implicated in human diseases.
Content updated September 2026.
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