What you carry at this position in your DNA and what research says about it.
Lipid Levels and Statins: 10/10 evidence, 16 publications.
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Sample genotype (not yours): C/C
Typical HDL and Favorable Statin Response
Standard lipid levels are expected, alongside a highly favorable response to common statin therapies. The risk for macular degeneration is naturally lower.
What this genotype means: Typical HDL cholesterol levels; Favorable response to statin therapy; Lower risk of macular degeneration.
Sample genotype (not yours): A/A
Higher HDL but Poorer Statin Response
Naturally higher levels of protective HDL cholesterol characterize this profile, though standard statin medications may be less effective at lowering overall cholesterol.
What this genotype means: Higher HDL cholesterol levels; Reduced cholesterol-lowering response to statins; Increased risk of macular degeneration.
Sample genotype (not yours): C/A
Typical Cholesterol and Statin Response
A balanced lipid profile is common, with slightly elevated HDL cholesterol levels. Standard statin medications generally perform with typical efficacy.
What this genotype means: Slightly higher HDL cholesterol; Typical response to statin therapy; Slightly higher risk of macular degeneration.
Gene function and biological role
Gene Function: The CETP gene encodes cholesteryl ester transfer protein, which plays a critical role in remodeling plasma lipoproteins [1]. This protein facilitates the exchange of cholesteryl esters from high-density lipoproteins to very-low-density and low-density lipoproteins [1]. Through this transfer process, CETP directly influences the balance of circulating cholesterol and lipoprotein particle sizes [2]. Variations in this gene can alter CETP activity, leading to significant differences in blood lipid profiles across populations [3]. Consequently, CETP is a major genetic determinant of cardiovascular health and a target for lipid-modifying therapies [4].
Variant Impact: Located within an intron of the CETP gene, rs1532624 is a common single nucleotide polymorphism that influences gene expression and protein function [5]. The nucleotide change from cytosine to adenine is associated with reduced CETP activity, which alters the rate of cholesterol transfer between lipoprotein particles [5]. This functional shift leads to elevated levels of cardioprotective HDL cholesterol in carriers of the minor allele [4]. However, the same genetic change also impacts how the liver processes lipids under certain therapeutic conditions, modifying the efficacy of standard cholesterol-lowering medications [6].
Key Insight: The same genetic variant that naturally boosts protective HDL cholesterol levels also makes standard statin medications less effective at lowering overall cholesterol.
Location: CETP. Chromosome 16 · 16q13 · 57.0 Mb
Estimated prevalence by population
Global 44.6%; European 31.2%; African 72.5%; East Asian 51.4%; South Asian 27.5%; Americas 43.0%; Ashkenazi 37.2%; Finnish 33.3%; Middle Eastern 39.6%; Amish 22.5%.
Estimated CC genotype frequency.
Global 41.9%; European 49.3%; African 25.3%; East Asian 40.6%; South Asian 49.9%; Americas 45.2%; Ashkenazi 47.6%; Finnish 48.8%; Middle Eastern 46.7%; Amish 49.9%.
Estimated CA genotype frequency.
Global 13.5%; European 19.5%; African 2.2%; East Asian 8.0%; South Asian 22.6%; Americas 11.9%; Ashkenazi 15.2%; Finnish 17.9%; Middle Eastern 13.7%; Amish 27.6%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 10/10. Source: PMID 19060911. Typical Levels.
Triglycerides. Evidence: 3/10. Source: PMID 35884923. Higher Levels.
Pharmacogenomics
Lipid-Lowering Drug Response
Statin Response. Evidence: 5/10. Source: PMID 20195290. Typical Response.
Organ Systems
Vision & Eye Health
Macular Degeneration. Evidence: 6/10. Source: PMID 39024449. Lower Risk.
Showing effects for A/A genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 19060911. Higher Levels.
Triglycerides. Evidence: 3/10. Source: PMID 35884923. Lower Levels.
Statin Response. Evidence: 5/10. Source: PMID 20195290. Poorer Response.
Macular Degeneration. Evidence: 6/10. Source: PMID 39024449. Higher Risk.
Showing effects for C/A genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 19060911. Slightly Higher.
Triglycerides. Evidence: 3/10. Source: PMID 35884923. Slightly Higher.
Macular Degeneration. Evidence: 6/10. Source: PMID 39024449. Slightly Higher Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Standard levels of high-density lipoprotein (HDL) cholesterol are typical for this common homozygous genotype [1]. Fully active cholesteryl ester transfer protein efficiently exchanges lipids between lipoprotein fractions, maintaining baseline HDL clearance rates [2]. Although this active state is linked to slightly higher circulating triglycerides, it also correlates with a lower risk of age-related macular degeneration. Most notably, clinical evidence demonstrates a highly effective response to standard statin medications [3]. HMG-CoA reductase inhibitors achieve optimal lipid-lowering results, significantly reducing total cholesterol levels in these individuals. Consequently, standard cardiovascular prevention guidelines and routine lipid management therapies remain highly effective [2].
Typical HDL cholesterol levels; Favorable response to statin therapy; Lower risk of macular degeneration.
Sample genotype: AA (Homozygous)
Elevated high-density lipoprotein (HDL) cholesterol levels are strongly associated with this double-variant genotype [1]. Reduced activity of the cholesteryl ester transfer protein slows the clearance of HDL particles, allowing them to accumulate in the bloodstream [2]. While higher HDL is generally considered favorable for cardiovascular health, clinical studies indicate a reduced lipid-lowering response to HMG-CoA reductase inhibitors, commonly known as statins [3]. Specifically, individuals with this genotype experience a smaller reduction in total cholesterol when prescribed standard statin therapies. Additionally, this genetic line is associated with an increased susceptibility to age-related macular degeneration [4]. Managing cardiovascular risk may therefore require personalized therapeutic strategies or alternative lipid-lowering agents [5].
Higher HDL cholesterol levels; Reduced cholesterol-lowering response to statins; Increased risk of macular degeneration.
Sample genotype: CA (Heterozygous)
Carrying one copy of the variant allele results in intermediate cholesteryl ester transfer protein activity [1]. This moderate protein function translates to slightly higher HDL cholesterol levels compared to the common baseline [2]. Triglyceride levels remain within a typical range, showing only a minor upward trend associated with the single cytosine allele [3]. Efficacy of HMG-CoA reductase inhibitors, or statins, is generally preserved, allowing for standard cholesterol-lowering responses [4]. While there is a slightly higher risk of age-related macular degeneration compared to non-carriers, the absolute impact remains modest [5]. Overall, this heterozygous state represents a balanced genetic influence on lipid metabolism and cardiovascular markers [1].
Slightly higher HDL cholesterol; Typical response to statin therapy; Slightly higher risk of macular degeneration.
Variants with shared genetic architecture
rs12720922 · CETP Gene · Chr 16 · Cholesterol and Heart Health
rs17231506 · CETP Gene · Chr 16 · Cardiovascular Health
rs173539 · CETP Gene · Chr 16 · Cholesterol Levels
Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts.
Genomic study in Mexicans identifies a new locus for triglycerides and refines European lipid loci.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Dyslipidaemia-Genotype Interactions with Nutrient Intake and Cerebro-Cardiovascular Disease.
Content updated August 2026.
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