What you carry at this position in your DNA and what research says about it.
Cholesterol Levels: 10/10 evidence, 28 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): C/C
Typical Cholesterol and Lipid Levels
Baseline levels of cholesteryl ester transfer protein result in typical lipid profiles. There is no inherited reduction in cardiovascular risk from this specific genetic marker.
What this genotype means: Typical HDL and LDL cholesterol levels; Standard baseline risk for coronary artery disease.
Sample genotype (not yours): C/T
Favorable Cholesterol Profile and Lower Heart Risk
A single copy of the protective variant reduces CETP levels, leading to higher HDL and lower LDL cholesterol. This shift supports overall cardiovascular health and a slightly lower risk of heart disease.
What this genotype means: Favorable lipid profile with higher HDL and lower LDL; Slightly reduced risk of coronary artery disease.
Sample genotype (not yours): T/T
Optimal Cholesterol Profile and Lowest Heart Risk
A double dose of the protective variant significantly lowers CETP levels, maximizing protective HDL and minimizing LDL cholesterol. This genetic profile is strongly linked to superior cardiovascular health.
What this genotype means: Highly favorable lipid profile with maximized HDL; Lowest genetic risk of coronary artery disease at this locus.
Gene function and biological role
Gene Function: The CETP gene encodes the cholesteryl ester transfer protein, a key player in lipid metabolism [1]. This protein facilitates the exchange of cholesteryl esters from high-density lipoproteins to very-low-density and low-density lipoproteins [1]. High levels of CETP activity lead to lower circulating levels of protective HDL cholesterol and higher levels of atherogenic LDL cholesterol [1]. Consequently, genetic variations that naturally lower CETP levels or activity are of great interest for cardiovascular health [2].
Variant Impact: Located in the promoter region of the CETP gene, rs247616 is a single-nucleotide variant that directly influences gene expression [3]. The minor T allele disrupts transcription factor binding, which reduces the production of CETP in the liver and spleen [3]. This reduction in circulating CETP levels leads to a significant increase in protective HDL cholesterol and a decrease in LDL cholesterol and triglycerides [4]. Because of its strong, direct effect on lipid profiles, this variant is widely studied as a natural model for CETP inhibition therapies [1].
Key Insight: Naturally lower levels of CETP mimic the effects of cholesterol-lowering medications currently in clinical development.
Location: CETP. Chromosome 16 · 16q13 · 57.0 Mb
Estimated prevalence by population
Global 50.4%; European 45.8%; African 55.4%; East Asian 69.7%; South Asian 44.4%; Americas 50.9%; Ashkenazi 54.0%; Finnish 52.5%; Middle Eastern 58.4%; Amish 37.3%.
Estimated CC genotype frequency.
Global 41.0%; European 43.8%; African 38.1%; East Asian 27.6%; South Asian 44.5%; Americas 40.9%; Ashkenazi 39.0%; Finnish 39.9%; Middle Eastern 36.1%; Amish 47.5%.
Estimated CT genotype frequency.
Global 8.6%; European 10.5%; African 6.5%; East Asian 2.7%; South Asian 11.1%; Americas 8.2%; Ashkenazi 7.0%; Finnish 7.6%; Middle Eastern 5.6%; Amish 15.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
CETP Levels. Evidence: 6/10. Source: PMID 29728394. Typical Levels.
Heart Disease
Coronary Artery Disease. Evidence: 7/10. Source: PMID 28714975. Typical Risk.
Pharmacogenomics
Lipid-Lowering Drug Response
Statin Response. Evidence: 6/10. Source: PMID 27587472. Typical Response.
Showing effects for C/T genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Higher Levels.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Lower Levels.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Lower Levels.
CETP Levels. Evidence: 6/10. Source: PMID 29728394. Lower Levels.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 28714975. Lower Risk.
Statin Response. Evidence: 6/10. Source: PMID 27587472. Better HDL Response.
Showing effects for T/T genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Significantly Higher.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Significantly Lower.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Significantly Lower.
CETP Levels. Evidence: 6/10. Source: PMID 29728394. Significantly Lower.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 28714975. Lowest Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Baseline activity of the cholesteryl ester transfer protein is maintained with this genotype [1]. This typical activity level facilitates the standard exchange of lipids between lipoprotein particles, resulting in average circulating levels of HDL and LDL cholesterol [1]. Large-scale genetic studies show that this typical lipid profile is associated with standard baseline risks for coronary artery disease [2]. While there is no elevated genetic risk, there is also no inherited protective effect against cardiovascular events [2]. Standard lifestyle factors and routine lipid panels remain the primary indicators of cardiovascular health.
Typical HDL and LDL cholesterol levels; Standard baseline risk for coronary artery disease.
Sample genotype: CT (Heterozygous)
Production of the cholesteryl ester transfer protein is partially reduced due to the presence of one protective allele [1]. This reduction limits the transfer of cholesterol from protective HDL particles to atherogenic LDL particles [1]. Consequently, clinical data associates this genotype with higher circulating levels of HDL cholesterol and lower levels of LDL cholesterol and triglycerides [2]. These favorable lipid shifts contribute to a slightly lower lifetime risk of developing coronary artery disease [3]. Additionally, some research suggests a more pronounced increase in HDL cholesterol when undergoing statin therapy [4].
Favorable lipid profile with higher HDL and lower LDL; Slightly reduced risk of coronary artery disease.
Sample genotype: TT (Homozygous)
Circulating levels of cholesteryl ester transfer protein are significantly decreased with two copies of the protective variant [1]. This substantial reduction in CETP activity preserves high levels of protective HDL cholesterol in the bloodstream while lowering LDL cholesterol and triglycerides [2]. Large multi-ethnic cohorts consistently demonstrate that these optimal lipid patterns translate to the lowest risk of coronary artery disease at this locus [3]. The metabolic profile closely mirrors the therapeutic goals of modern lipid-lowering drugs [1]. Furthermore, individuals with this genotype may experience an enhanced HDL-raising response when treated with statins [4].
Highly favorable lipid profile with maximized HDL; Lowest genetic risk of coronary artery disease at this locus.
Variants with shared genetic architecture
rs12720922 · CETP Gene · Chr 16 · Cholesterol and Heart Health
rs1532624 · CETP Gene · Chr 16 · Lipid Levels and Statins
rs17231506 · CETP Gene · Chr 16 · Cardiovascular Health
Association analyses based on false discovery rate implicate new loci for coronary artery disease.
A large electronic-health-record-based genome-wide study of serum lipids.
Meta-analysis of genome-wide association studies of HDL cholesterol response to statins.
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