What you carry at this position in your DNA and what research says about it.
Hormone and Drug Metabolism: 9/10 evidence, 24 publications.
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Sample genotype (not yours): T/T
Typical Hormone and Drug Metabolism
Normal silencing of the fetal CYP3A7 gene occurs after birth, resulting in typical hormone levels and standard drug clearance.
What this genotype means: Typical baseline hormone levels; Standard clearance of statins and chemotherapy; Slightly higher baseline risk of gout compared to G carriers.
Sample genotype (not yours): G/G
Significantly Altered Hormones and Rapid Drug Clearance
Carrying two copies of the G allele leads to highly active adult CYP3A7 expression, lowering hormone levels and rapidly clearing medications.
What this genotype means: Lowest circulating sex hormone levels; Substantially reduced risk of developing hormone-positive breast cancer; Highly accelerated clearance of CYP3A-metabolized medications.
Sample genotype (not yours): T/G
Altered Hormone Levels and Faster Drug Clearance
Active adult expression of the CYP3A7 gene lowers sex hormone levels, reducing breast cancer risk but potentially accelerating drug clearance.
What this genotype means: Lower circulating estrogen and progesterone; Reduced risk of developing hormone-positive breast cancer; Faster clearance of certain chemotherapy drugs and statins.
Gene function and biological role
Gene Function: The CYP3A7 gene encodes an enzyme that is part of the cytochrome P450 family, which is responsible for clearing various hormones and drugs from the body [1]. Under normal circumstances, this specific gene is highly active during fetal development but is silenced shortly after birth [2]. In adults, other enzymes like CYP3A4 typically take over these metabolic duties. However, certain genetic variations can cause the CYP3A7 gene to remain active throughout adulthood, altering how sex hormones and medications are processed [2]. This persistent adult expression can significantly lower circulating hormone levels and accelerate the clearance of certain therapeutic drugs [1] [2].
Variant Impact: This variant, rs45446698, is an intronic change that serves as the primary genetic tag for the CYP3A7*1C allele [2]. Carrying the G allele prevents the normal silencing of the CYP3A7 gene after birth, leading to active enzyme production in adult tissues [2]. This active adult enzyme rapidly breaks down sex steroids, including estrogen, progesterone, and testosterone, resulting in lower circulating levels of these hormones [2]. Additionally, the presence of this active enzyme in adults can lead to the rapid breakdown of various medications, including some chemotherapy drugs and statins [1].
Key Insight: This variant acts as a genetic switch that keeps a fetal gene active in adulthood, which simultaneously lowers natural hormone levels and speeds up the clearance of common medications.
Location: CYP3A7. Chromosome 7 · 7q22.1 · 99.7 Mb
Estimated prevalence by population
Global 94.8%; European 93.0%; African 98.0%; East Asian 100.0%; South Asian 97.2%; Americas 94.5%; Ashkenazi 94.3%; Finnish 90.8%; Middle Eastern 94.6%; Amish 98.5%.
Estimated TT genotype frequency.
Global 5.1%; European 6.8%; African 1.9%; East Asian 0.0%; South Asian 2.7%; Americas 5.5%; Ashkenazi 5.6%; Finnish 9.0%; Middle Eastern 5.3%; Amish 1.5%.
Estimated TG genotype frequency.
Global 0.1%; European 0.1%; African < 0.1%; East Asian 0.0%; South Asian < 0.1%; Americas 0.1%; Ashkenazi 0.1%; Finnish 0.2%; Middle Eastern 0.1%; Amish < 0.1%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Endocrine & Reproductive
Hormone Levels & Endocrine Regulation
Hormone Levels. Evidence: 9/10. Source: PMID 33495599. Typical Levels.
Cancer & Oncology
Cancer Prognosis & Treatment Outcome
Cancer Prognosis. Evidence: 3/10. Source: PMID 33495599. Typical Prognosis.
Breast Cancer
Breast Cancer. Evidence: 3/10. Source: PMID 33495599. Typical Risk.
Organ Systems
Bone, Joint & Connective Tissue Health
Bone Mineral Density. Evidence: 8/10. Source: PMID 30048462. Typical Density.
Cardiovascular & Metabolic
Gout & Uric Acid
Gout. Evidence: 6/10. Source: PMID 39406924. Slightly Higher Risk.
Pharmacogenomics
Lipid-Lowering Drug Response
Atorvastatin Clearance. Evidence: 5/10. Source: PMID 32128760. Typical Metabolism.
Showing effects for G/G genotype
Hormone Levels. Evidence: 9/10. Source: PMID 33495599. Lowest Hormones.
Cancer Prognosis. Evidence: 3/10. Source: PMID 33495599. Worse Outcomes.
Breast Cancer. Evidence: 3/10. Source: PMID 33495599. Reduced Risk.
Bone Mineral Density. Evidence: 8/10. Source: PMID 30048462. Lower Density.
Gout. Evidence: 6/10. Source: PMID 39406924. Lower Risk.
Atorvastatin Clearance. Evidence: 5/10. Source: PMID 32128760. Faster Metabolism.
Showing effects for T/G genotype
Hormone Levels. Evidence: 9/10. Source: PMID 33495599. Lower Hormones.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Typical silencing of the fetal CYP3A7 gene occurs shortly after birth, meaning adult metabolic processes rely on other standard enzymes [1]. Because this fetal enzyme is not active, sex hormones such as estrogen, progesterone, and testosterone are processed at a standard rate, maintaining typical baseline levels [1]. This typical hormone profile is associated with standard bone mineral density and a baseline risk for hormone-sensitive conditions [2]. However, typical hormone levels mean there is no genetically driven reduction in the risk of developing hormone receptor-positive breast cancer compared to G allele carriers [1]. Additionally, typical levels of uric acid processing result in a slightly higher baseline risk of gout compared to those who carry the minor G allele [3]. Medications, including statins and standard chemotherapies, are metabolized at normal, expected rates [4].
Typical baseline hormone levels; Standard clearance of statins and chemotherapy; Slightly higher baseline risk of gout compared to G carriers.
Sample genotype: GG (Homozygous)
Highly active adult expression of the fetal CYP3A7 gene occurs due to carrying two copies of the G allele [1]. This double-copy status leads to the most pronounced reduction in sex hormones, including estrogen, progesterone, and testosterone, due to rapid enzymatic breakdown [1]. While these lower hormone levels significantly decrease the risk of developing hormone receptor-positive breast cancer, they also present distinct physiological trade-offs [1]. Specifically, the reduction in sex hormones is linked to lower bone mineral density, which may elevate the risk of osteoporosis and fractures [2]. In the context of cancer treatment, this genotype is associated with accelerated clearance of chemotherapy agents that are CYP3A substrates, which can reduce treatment efficacy and worsen survival outcomes [1]. Furthermore, individuals with this genotype metabolize atorvastatin much faster and have a lower risk of developing gout [3] [4].
Lowest circulating sex hormone levels; Substantially reduced risk of developing hormone-positive breast cancer; Highly accelerated clearance of CYP3A-metabolized medications.
Sample genotype: TG (Heterozygous)
Persistent adult expression of the fetal CYP3A7 gene occurs due to carrying one copy of the G allele [1]. This active enzyme rapidly breaks down sex hormones, resulting in significantly lower levels of premenopausal estrogen, progesterone, and testosterone [1]. Lower hormone levels provide a protective effect, reducing the risk of developing hormone receptor-positive breast cancer [1]. However, this hormonal reduction can also lead to lower bone mineral density, potentially increasing the long-term risk of osteoporosis [2]. If diagnosed with certain cancers like breast cancer, lung cancer, or leukemia, carrying this allele is linked to poorer treatment outcomes and higher mortality [1]. This is because the active enzyme can rapidly clear chemotherapy drugs that are CYP3A substrates, making standard doses less effective [1]. Additionally, this genotype is associated with faster metabolism of atorvastatin and a lower risk of gout [3] [4].
Lower circulating estrogen and progesterone; Reduced risk of developing hormone-positive breast cancer; Faster clearance of certain chemotherapy drugs and statins.
Variants with shared genetic architecture
rs2257401 · CYP3A7 Gene · Chr 7 · Immunosuppressant Metabolism
rs1799941 · SHBG Gene · Chr 17 · Hormone Binding Globulin
rs56196860 · FKBP4 Gene · Chr 12 · Hormone and Metabolic Health
A Genome-wide Association Study of Circulating Levels of Atorvastatin and Its Major Metabolites.
A genome-wide association analysis reveals new pathogenic pathways in gout.
Content updated August 2026.
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