What you carry at this position in your DNA and what research says about it.
Tuberculosis Drug Liver Risk: 5/10 evidence, 30 publications.
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Sample genotype (not yours): C/C
Higher Risk of Drug-Induced Liver Injury
Standard enzyme activity leads to rapid processing of certain medications, which can generate harmful byproducts. This increases the likelihood of liver irritation when taking specific treatments like anti-tuberculosis drugs.
What this genotype means: Higher risk of liver damage from anti-tuberculosis drugs; Slightly increased susceptibility to certain cancers.
Sample genotype (not yours): C/T
Lower Risk of Drug-Induced Liver Injury
Reduced enzyme activity slows down the conversion of certain drugs into toxic byproducts. This provides a protective effect against liver damage during specific medical treatments.
What this genotype means: Reduced risk of liver damage from anti-tuberculosis drugs; Slightly lower susceptibility to certain cancers.
Sample genotype (not yours): T/T
Lowest Risk of Drug-Induced Liver Injury
Significantly lower enzyme activity minimizes the generation of toxic drug byproducts. This offers the strongest genetic protection against liver damage from specific medications.
What this genotype means: Lowest risk of liver damage from anti-tuberculosis drugs; Lower susceptibility to certain cancers.
Gene function and biological role
Gene Function: The CYP2E1 gene encodes cytochrome P450 2E1, a key enzyme in the liver that metabolizes a wide range of foreign compounds [1]. This enzyme is responsible for processing small molecules, including alcohol, industrial solvents like benzene, and several prescription medications [2]. During this metabolic process, CYP2E1 can convert otherwise harmless substances into highly reactive, toxic intermediates or carcinogens [3]. Consequently, the activity level of this gene plays a critical role in determining susceptibility to chemical-induced liver damage and certain cancers [4].
Variant Impact: The rs2031920 variant is located in the promoter region of the CYP2E1 gene and alters its transcriptional activity [5]. The minor T allele, also known as the c2 or CYP2E1-1055C>T variant, disrupts a binding site for transcription factors, leading to reduced expression of the enzyme [5]. Because the T allele decreases enzyme levels, carriers produce fewer toxic metabolites when exposed to certain drugs and environmental toxins [3]. This reduction in metabolic activation generally lowers the risk of liver injury and chemical-induced cancers compared to the common C allele [6].
Key Insight: The variant T allele reduces the liver's production of toxic drug byproducts, turning what is normally a low-activity enzyme variant into a protective shield against medication-induced liver damage.
Location: CYP2E1. Chromosome 10 · 10q26.3 · 133.5 Mb
Estimated prevalence by population
Global 93.6%; European 94.8%; African 98.5%; East Asian 63.3%; South Asian 97.5%; Americas 83.1%; Ashkenazi 89.9%; Finnish 95.7%; Middle Eastern 98.6%; Amish 94.4%.
Estimated CC genotype frequency.
Global 6.2%; European 5.1%; African 1.5%; East Asian 32.5%; South Asian 2.5%; Americas 16.1%; Ashkenazi 9.8%; Finnish 4.3%; Middle Eastern 1.4%; Amish 5.6%.
Estimated CT genotype frequency.
Global 0.3%; European 0.1%; African < 0.1%; East Asian 4.2%; South Asian < 0.1%; Americas 0.8%; Ashkenazi 0.3%; Finnish < 0.1%; Middle Eastern < 0.1%; Amish 0.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Antimicrobial & Antiviral Response
Tuberculosis Drug Liver Injury. Evidence: 5/10. Source: PMID 12668988. Increased Risk.
Cancer & Oncology
Head, Neck & Oral Cancers
Nasopharyngeal Cancer. Evidence: 3/10. Source: PMID 26582733. Increased Risk.
Gastrointestinal Cancers
Gastric Cancer. Evidence: 3/10. Source: PMID 26373042. Increased Risk.
Colorectal Cancer
Colorectal Cancer. Evidence: 3/10. Source: PMID 23595220. Lower Risk.
Showing effects for C/T genotype
Tuberculosis Drug Liver Injury. Evidence: 5/10. Source: PMID 12668988. Decreased Risk.
Nasopharyngeal Cancer. Evidence: 3/10. Source: PMID 26582733. Decreased Risk.
Gastric Cancer. Evidence: 3/10. Source: PMID 26373042. Decreased Risk.
Colorectal Cancer. Evidence: 3/10. Source: PMID 23595220. Increased Risk.
Showing effects for T/T genotype
Colorectal Cancer. Evidence: 3/10. Source: PMID 23595220. Higher Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Standard enzyme levels are maintained by this genotype, resulting in typical metabolic processing of foreign compounds [1]. When taking anti-tuberculosis medications such as isoniazid or rifampin, this active state can rapidly convert the drugs into toxic hydrazine intermediates [2]. These reactive compounds can accumulate and cause significant stress to liver cells, raising the risk of drug-induced liver injury [3]. Additionally, standard enzyme activity is associated with a slightly higher susceptibility to certain cancers, such as nasopharyngeal and gastric cancers, due to the activation of environmental pro-carcinogens [4]. Avoiding excessive alcohol consumption and minimizing exposure to industrial solvents like benzene can help protect liver health [5].
Higher risk of liver damage from anti-tuberculosis drugs; Slightly increased susceptibility to certain cancers.
Sample genotype: CT (Heterozygous)
Enzyme expression is reduced by the presence of one copy of the variant allele, which alters transcription factor binding in the promoter [1]. This reduction in enzyme levels slows the rate at which medications like isoniazid are converted into toxic metabolites [2]. Consequently, liver cells are exposed to fewer reactive compounds, lowering the risk of drug-induced hepatotoxicity during tuberculosis therapy [3]. This slower metabolic activation also offers a protective shield against certain cancers, such as nasopharyngeal cancers, by reducing the activation of dietary and environmental carcinogens [4]. However, overall drug clearance and liver health can still be influenced by other genetic factors and lifestyle choices [5].
Reduced risk of liver damage from anti-tuberculosis drugs; Slightly lower susceptibility to certain cancers.
Sample genotype: TT (Homozygous)
Enzyme activity is at its lowest because both copies of the gene carry the promoter variant [1]. This significant reduction in enzyme levels prevents the rapid accumulation of toxic intermediates from medications like isoniazid and rifampin [2]. As a result, the liver is highly protected against drug-induced hepatitis during standard tuberculosis treatment regimens [3]. Furthermore, the minimal activation of pro-carcinogens like nitrosamines translates to a lower susceptibility to various cancers, including gastric and nasopharyngeal cancers [4]. While this genotype is highly protective against chemical-induced liver injury, individuals should still discuss all medication plans with their healthcare provider [5].
Lowest risk of liver damage from anti-tuberculosis drugs; Lower susceptibility to certain cancers.
Variants with shared genetic architecture
rs6413432 · CYP2E1 Gene · Chr 10 · Drug Metabolism and Toxicity
rs3813867 · CYP2E1 Gene · Chr 10 · Liver Health and Cancer Risk
rs2070673 · CYP2E1 Gene · Chr 10 · Liver and Chemical Safety
Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis.
[Genetic polymorphism of cytochrome P450 2E1 and the risk of nasopharyngeal carcinoma].
Content updated August 2026.
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