What you carry at this position in your DNA and what research says about it.
Toxin Detoxification: 7/10 evidence, 63 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): G/G
Typical Detoxification and Standard Cancer Risk
Fully functional NQO1 enzyme activity provides normal protection against environmental toxins. This profile represents the typical baseline for cancer risk and medication responses.
What this genotype means: Normal NQO1 enzyme activity; Standard baseline cancer risk; Typical response to chemotherapy.
Sample genotype (not yours): A/A
Impaired Detoxification and Elevated Chemical Sensitivity
A near-complete loss of NQO1 enzyme activity significantly increases susceptibility to environmental toxins like benzene. This profile is linked to higher risks of certain cancers and altered chemotherapy outcomes.
What this genotype means: Near-complete loss of NQO1 activity; Increased sensitivity to benzene and pollutants; Higher risk of certain cancers.
Sample genotype (not yours): G/A
Reduced Detoxification with Mixed Cancer Risks
Moderately reduced NQO1 enzyme activity occurs with this genetic profile. It is associated with a lower risk of lung cancer but potentially poorer responses to certain chemotherapy drugs.
What this genotype means: Moderately reduced enzyme activity; Lower risk of lung cancer; Altered chemotherapy response.
Gene function and biological role
Gene Function: The NQO1 gene encodes NAD(P)H quinone dehydrogenase 1, a crucial phase II detoxification enzyme [1]. This enzyme primarily functions as an antioxidant, protecting cells from oxidative stress by neutralizing highly reactive quinones and quinone-imines into safer, less toxic hydroquinones [2]. It is highly active in tissues exposed to the environment, such as the lungs, breast, and colon, where it provides a vital line of defense against cellular damage [2]. Additionally, NQO1 plays a key role in stabilizing tumor-suppressor proteins like p53, preventing their premature degradation [1]. When NQO1 function is impaired, reactive compounds can accumulate, leading to increased DNA damage and oxidative stress [1].
Variant Impact: The rs1800566 variant, also known as NQO1*2 or C609T, is a missense mutation that changes the amino acid proline to serine at position 187 of the enzyme [2]. This single-letter change makes the resulting NQO1 protein extremely unstable, causing it to be rapidly targeted for degradation by the body's proteasome system [2]. As a result, individuals carrying the variant allele experience a significant reduction in NQO1 enzyme levels and activity [3]. Those with two copies of the variant allele have virtually undetectable NQO1 activity, leaving cells highly vulnerable to environmental toxins [2]. This lack of functional enzyme impairs the detoxification of harmful chemicals like benzene and alters responses to several chemotherapy drugs [3].
Key Insight: The NQO1*2 variant causes the enzyme to become so unstable that the body's cellular cleanup crew immediately destroys it, leaving some individuals with zero functional NQO1 activity.
Location: NQO1. Chromosome 16 · 16q22.1 · 69.7 Mb
Estimated prevalence by population
Global 61.8%; European 65.6%; African 66.2%; East Asian 30.8%; South Asian 44.3%; Americas 45.1%; Ashkenazi 67.5%; Finnish 65.8%; Middle Eastern 57.5%; Amish 63.5%.
Estimated GG genotype frequency.
Global 33.1%; European 30.8%; African 30.3%; East Asian 49.4%; South Asian 44.5%; Americas 44.1%; Ashkenazi 29.3%; Finnish 30.6%; Middle Eastern 36.6%; Amish 32.3%.
Estimated GA genotype frequency.
Global 5.1%; European 3.6%; African 3.5%; East Asian 19.8%; South Asian 11.2%; Americas 10.8%; Ashkenazi 3.2%; Finnish 3.6%; Middle Eastern 5.8%; Amish 4.1%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Toxin Detoxification. Evidence: 3/10. Source: PMID 18214807. Normal Activity.
Chemotherapy Response
Chemotherapy Response. Evidence: 7/10. Source: PMID 18511948. Typical Response.
Anticoagulant & Blood Thinner Response
Warfarin Sensitivity. Evidence: 6/10. Source: PMID 26257249. Typical Sensitivity.
Cancer & Oncology
General Cancer Risk
Cancer Susceptibility. Evidence: 6/10. Source: PMID 18511948. Typical Risk.
Neurology & Mental Health
Addiction & Reward
Alcohol Consumption. Evidence: 7/10. Source: PMID 30679032. Typical Consumption.
Showing effects for A/A genotype
Toxin Detoxification. Evidence: 3/10. Source: PMID 18214807. Severely Impaired.
Chemotherapy Response. Evidence: 7/10. Source: PMID 18511948. Poorest Response.
Warfarin Sensitivity. Evidence: 6/10. Source: PMID 26257249. Higher Tolerance.
Cancer Susceptibility. Evidence: 6/10. Source: PMID 18511948. Increased Risk.
Alcohol Consumption. Evidence: 7/10. Source: PMID 30679032. Higher Consumption.
Showing effects for G/A genotype
Toxin Detoxification. Evidence: 3/10. Source: PMID 18214807. Moderately Reduced.
Chemotherapy Response. Evidence: 7/10. Source: PMID 18511948. Poorer Response.
Cancer Susceptibility. Evidence: 6/10. Source: PMID 18511948. Lower Lung Cancer.
Alcohol Consumption. Evidence: 7/10. Source: PMID 30679032. Slightly Higher.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Production of the NQO1 enzyme remains fully functional when two copies of the G allele are present, ensuring efficient neutralization of reactive chemical compounds [1]. Normal enzyme activity helps shield cells from oxidative stress and DNA damage caused by everyday environmental exposures [1]. Clinical data indicate a standard baseline risk for various cancers, including lung and gastrointestinal cancers, under this genetic profile [2]. Standard responses to common chemotherapy drugs and a typical response to medications like warfarin are also expected [3]. Representing the most common genetic profile globally, this status offers stable cellular defense mechanisms [1]. Cells are able to process quinones efficiently, preventing them from turning into destructive reactive oxygen species. This baseline level of protection is considered optimal for general health and environmental resilience.
Normal NQO1 enzyme activity; Standard baseline cancer risk; Typical response to chemotherapy.
Sample genotype: AA (Homozygous)
Two copies of the A allele cause the NQO1 enzyme to become highly unstable, leading to its rapid degradation and virtually undetectable activity levels in the body [1]. Cells are significantly less equipped to neutralize reactive quinones without functional NQO1, leading to elevated oxidative stress and DNA damage [1]. Impaired detoxification dramatically increases susceptibility to toxic chemicals, particularly benzene, which is found in vehicle exhaust, tobacco smoke, and industrial environments [2]. Clinical research associates this genotype with an increased risk of developing certain cancers, such as colorectal and bladder cancers [3]. Furthermore, the lack of NQO1 activity strongly impacts cancer treatment, predicting poorer survival rates and poorer responses to several chemotherapy drugs, including epirubicin and cisplatin [4]. It may also alter the response to the blood thinner warfarin [5]. This complete absence of enzyme activity means that avoiding unnecessary chemical exposures is highly beneficial. Alternative antioxidant support through diet and lifestyle may help mitigate the increased cellular stress.
Near-complete loss of NQO1 activity; Increased sensitivity to benzene and pollutants; Higher risk of certain cancers; Poorer response to specific chemotherapies.
Sample genotype: GA (Heterozygous)
A moderate reduction in NQO1 enzyme levels occurs when one copy of the A allele is inherited, as the variant protein is less stable than the reference form [1]. Partial reduction can slightly lower the body's efficiency in clearing certain environmental toxins, such as benzene [2]. Clinical studies suggest that this heterozygous profile may actually offer a significantly reduced risk of developing lung cancer [3]. However, the same reduction in enzyme activity is also linked to poorer clinical outcomes and altered toxicity profiles when undergoing specific chemotherapy regimens, such as those containing fluorouracil or epirubicin [4]. It also influences the metabolism of other medications, potentially producing a weaker response to the blood thinner warfarin [5]. The body must rely on alternative antioxidant pathways to compensate for the partial loss of NQO1 activity. While daily health is rarely impacted, exposure to high levels of chemical pollutants can place extra stress on the cells.
Moderately reduced enzyme activity; Lower risk of lung cancer; Altered chemotherapy response.
Variants with shared genetic architecture
rs1131341 · NQO1 Gene · Chr 16 · Detoxification and Cancer Risk
rs1051740 · EPHX1 Gene · Chr 1 · Toxin Detoxification
rs3957357 · GSTA1 Gene · Chr 6 · Detoxification Capacity
A functional NQO1 609C>T polymorphism and risk of gastrointestinal cancers: a meta-analysis.
Tobacco and estrogen metabolic polymorphisms and risk of non-small cell lung cancer in women.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com