What you carry at this position in your DNA and what research says about it.
Drug Metabolism and Toxicity: 6/10 evidence, 11 publications.
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Sample genotype (not yours): T/T
Better Chemotherapy Survival and Typical Drug Toxicity Risk
This genotype is associated with increased survival rates when undergoing certain chemotherapy treatments. It also correlates with a typical, baseline risk of liver toxicity from common tuberculosis medications.
What this genotype means: Typical drug metabolism; Higher survival rates on cisplatin; Baseline risk of liver toxicity.
Sample genotype (not yours): A/A
Highest Drug Toxicity and Lower Chemotherapy Survival
Carrying two copies of the minor allele is linked to slower metabolism of isoniazid and a significantly higher risk of liver damage from tuberculosis treatments. It is also associated with reduced survival rates during cisplatin-based chemotherapy and increased paclitaxel side effects.
What this genotype means: Significantly slower drug clearance; Highest risk of drug-induced liver damage; Lower survival rates on cisplatin.
Sample genotype (not yours): T/A
Increased Drug Toxicity and Lower Chemotherapy Survival
Carrying one copy of the minor allele is linked to a higher risk of liver damage from tuberculosis medications. It is also associated with reduced survival rates during cisplatin-based chemotherapy and increased side effects from paclitaxel.
What this genotype means: Slower drug clearance; Elevated risk of drug-induced liver damage; Lower survival rates on cisplatin.
Gene function and biological role
Gene Function: The CYP2E1 gene encodes cytochrome P450 2E1, a key enzyme in the liver that metabolizes various foreign compounds, including drugs, toxins, and dietary carcinogens [1]. It plays a critical role in activating procarcinogens into highly reactive intermediates that can damage DNA [2]. Variations in this gene can significantly alter enzyme activity, leading to differences in how individuals process medications and clear environmental toxins [3]. This enzyme is also involved in the metabolism of alcohol and is a major source of cellular oxidative stress [4].
Variant Impact: This intron variant, also known as the DraI polymorphism, alters a thymine to an adenine in the CYP2E1 gene [3]. The change affects the regulation of the enzyme, influencing how rapidly certain medications are metabolized in the liver [5]. It has been widely studied for its impact on the efficacy and side effects of chemotherapy drugs [6]. Additionally, it serves as a genetic marker for susceptibility to liver injury when taking standard tuberculosis therapies [7].
Key Insight: This variant significantly impacts the risk of liver damage from standard tuberculosis treatments and influences survival outcomes during cisplatin-based chemotherapy.
Location: CYP2E1. Chromosome 10 · 10q26.3 · 133.5 Mb
Estimated prevalence by population
Global 80.7%; European 82.8%; African 84.4%; East Asian 55.7%; South Asian 66.9%; Americas 76.3%; Ashkenazi 82.0%; Finnish 76.8%; Middle Eastern 93.3%; Amish 83.2%.
Estimated TT genotype frequency.
Global 18.1%; European 16.4%; African 14.9%; East Asian 37.9%; South Asian 29.8%; Americas 22.1%; Ashkenazi 17.1%; Finnish 21.7%; Middle Eastern 6.6%; Amish 16.0%.
Estimated TA genotype frequency.
Global 1.2%; European 0.8%; African 0.7%; East Asian 6.4%; South Asian 3.3%; Americas 1.6%; Ashkenazi 0.9%; Finnish 1.5%; Middle Eastern 0.1%; Amish 0.8%.
Estimated AA genotype frequency.
Showing effects for T/T genotype
Cancer & Oncology
Cancer Prognosis & Treatment Outcome
Chemotherapy Survival. Evidence: 5/10. Source: PMID 22188361. Increased Survival.
Pharmacogenomics
Antimicrobial & Antiviral Response
Isoniazid Toxicity. Evidence: 6/10. Source: PMID 16677176. Typical Risk.
Rifampin Toxicity. Evidence: 6/10. Source: PMID 16677176. Typical Risk.
Pyrazinamide Toxicity. Evidence: 6/10. Source: PMID 16677176. Typical Risk.
Chemotherapy Response
Paclitaxel Toxicity. Evidence: 5/10. Source: PMID 41148602. Typical Risk.
Showing effects for A/A genotype
Chemotherapy Survival. Evidence: 5/10. Source: PMID 22188361. Decreased Survival.
Isoniazid Toxicity. Evidence: 6/10. Source: PMID 16677176. Increased Risk.
Rifampin Toxicity. Evidence: 6/10. Source: PMID 16677176. Increased Risk.
Pyrazinamide Toxicity. Evidence: 6/10. Source: PMID 16677176. Increased Risk.
Paclitaxel Toxicity. Evidence: 5/10. Source: PMID 41148602. Increased Risk.
Showing effects for T/A genotype
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Standard enzymatic activity is maintained by this genotype, resulting in typical processing of many common medications [1]. When undergoing cisplatin-based chemotherapy, patients with this genotype exhibit significantly improved progression-free survival compared to those carrying the variant allele [2]. The risk of developing severe peripheral neuropathy or pain during paclitaxel treatment remains at the typical baseline level [3]. Similarly, the liver processes tuberculosis drugs like isoniazid, rifampin, and pyrazinamide at a normal rate [4]. This normal clearance rate helps prevent the toxic accumulation of drug metabolites, keeping the risk of drug-induced hepatitis low [5]. Overall, this genetic profile is highly favorable for standard chemotherapy outcomes and carries no elevated risk for drug-induced liver injury.
Typical drug metabolism; Higher survival rates on cisplatin; Baseline risk of liver toxicity.
Sample genotype: AA (Homozygous)
Slower drug clearance and altered metabolic pathways characterize this homozygous variant genotype [1]. Patients carrying two copies of the variant allele experience a significantly increased risk of liver toxicity when taking standard tuberculosis medications [2]. Isoniazid concentrations in the blood tend to be higher, which correlates with a greater likelihood of drug-induced hepatitis [3]. When undergoing chemotherapy with cisplatin or cyclophosphamide, this genotype is associated with reduced progression-free survival [4]. There is also a heightened susceptibility to paclitaxel-induced side effects, such as painful peripheral neuropathy [5]. These findings highlight the importance of personalized medicine and careful monitoring of liver health during intensive drug therapies.
Significantly slower drug clearance; Highest risk of drug-induced liver damage; Lower survival rates on cisplatin.
Sample genotype: TA (Heterozygous)
Enzymatic function is altered by carrying one copy of the variant allele, which can slow down the clearance of specific drugs [1]. During tuberculosis therapy with isoniazid, rifampin, or pyrazinamide, this slower metabolism is linked to a significantly higher risk of drug-induced liver damage [2]. The accumulation of toxic drug metabolites can lead to elevated liver enzymes and hepatitis [3]. When treated with cisplatin and cyclophosphamide for ovarian cancer, patients with this genotype show a decreased likelihood of progression-free survival [4]. Furthermore, paclitaxel chemotherapy is more likely to trigger adverse side effects, including severe neuropathy and pain [5]. Monitoring liver function and discussing alternative treatment regimens with a healthcare provider may be beneficial when these medications are prescribed.
Slower drug clearance; Elevated risk of drug-induced liver damage; Lower survival rates on cisplatin.
Variants with shared genetic architecture
rs2031920 · CYP2E1 Gene · Chr 10 · Tuberculosis Drug Liver Risk
rs3813867 · CYP2E1 Gene · Chr 10 · Liver Health and Cancer Risk
rs2070673 · CYP2E1 Gene · Chr 10 · Liver and Chemical Safety
Genotype and allele frequencies of polymorphic CYP2E1 in the Turkish population.
Content updated August 2026.
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