What you carry at this position in your DNA and what research says about it.
Heart Disease Risk: 8/10 evidence, 19 publications.
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Sample genotype (not yours): A/A
Typical Heart Disease Risk
This genotype is associated with a baseline risk of coronary heart disease. It does not carry the genetic variant that increases susceptibility to cardiovascular events.
What this genotype means: Typical baseline risk of coronary heart disease; Standard clinical response to pravastatin therapy.
Sample genotype (not yours): A/G
Increased Heart Disease Risk
Carrying one copy of the G variant is associated with an elevated risk of coronary events. However, it also predicts a significantly better response to pravastatin therapy.
What this genotype means: Elevated baseline risk of coronary heart disease; Enhanced clinical benefit from pravastatin therapy.
Sample genotype (not yours): G/G
Carrying two copies of the G variant is linked to higher cardiovascular risk, but also predicts a stronger preventative response to pravastatin.
What this genotype means: Elevated baseline risk of coronary heart disease and stroke; Enhanced clinical benefit from pravastatin therapy; Potentially altered lipid-lowering response to other statins.
Gene function and biological role
Gene Function: The KIF6 gene encodes kinesin family member 6, a molecular motor protein involved in the intracellular transport of organelles and protein complexes along microtubules. This transport system is critical for maintaining cellular structure and function within the vascular system. Variations in this gene can alter the protein's cargo-binding capacity, potentially affecting cellular health in blood vessels. Research has focused heavily on how these changes influence susceptibility to coronary events and individual responses to cholesterol-lowering medications [1]. Understanding these genetic differences helps clarify why some individuals experience different cardiovascular outcomes and drug efficacies [2].
Variant Impact: The rs20455 variant is a missense mutation in the KIF6 gene that causes an amino acid substitution from tryptophan to arginine at position 719 of the protein. This structural alteration, often designated as Trp719Arg, is hypothesized to modify the molecular motor's transport efficiency. Clinical studies have linked the arginine-encoding G allele to an elevated risk of coronary heart disease and myocardial infarction [1]. However, carriers of this variant also tend to show a significantly enhanced clinical benefit from certain statin therapies, particularly pravastatin [3]. Conversely, some studies suggest that the variant may reduce the direct lipid-lowering efficiency of other statins like simvastatin [4].
Key Insight: Carriers of the G allele have a higher baseline risk of heart disease, yet they paradoxically receive a much stronger protective benefit from pravastatin therapy compared to non-carriers.
Location: KIF6. Chromosome 6 · 6p21.2 · 39.4 Mb
Estimated prevalence by population
Global 29.8%; European 40.8%; African 4.1%; East Asian 27.3%; South Asian 30.8%; Americas 37.8%; Ashkenazi 43.7%; Finnish 42.7%; Middle Eastern 29.6%; Amish 44.9%.
Estimated AA genotype frequency.
Global 42.6%; European 46.1%; African 32.2%; East Asian 49.9%; South Asian 49.4%; Americas 47.4%; Ashkenazi 44.8%; Finnish 45.3%; Middle Eastern 49.6%; Amish 44.2%.
Estimated AG genotype frequency.
Global 27.6%; European 13.0%; African 63.7%; East Asian 22.8%; South Asian 19.8%; Americas 14.8%; Ashkenazi 11.5%; Finnish 12.0%; Middle Eastern 20.8%; Amish 10.9%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Heart Disease
Coronary Artery Disease. Evidence: 8/10. Source: PMID 18222353. Typical Risk.
Heart Attack. Evidence: 8/10. Source: PMID 18222353. Typical Risk.
Stroke
Stroke. Evidence: 3/10. Source: PMID 18799872. Typical Risk.
Pharmacogenomics
Lipid-Lowering Drug Response
Pravastatin Response. Evidence: 8/10. Source: PMID 18222353. Typical Response.
Showing effects for A/G genotype
Coronary Artery Disease. Evidence: 8/10. Source: PMID 18222353. Increased Risk.
Heart Attack. Evidence: 8/10. Source: PMID 18222353. ~1.3x Risk.
Stroke. Evidence: 3/10. Source: PMID 18799872. Increased Risk.
Pravastatin Response. Evidence: 8/10. Source: PMID 18222353. Stronger Response.
Showing effects for G/G genotype
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Individuals with this genotype carry two copies of the common A allele, which encodes the typical tryptophan residue at position 719 of the KIF6 protein. Clinical studies indicate that this genotype does not experience the elevated baseline risk of coronary heart disease or myocardial infarction associated with the variant G allele [1]. However, clinical trials also suggest that individuals with this genotype may derive less relative cardiovascular event reduction from standard pravastatin therapy compared to G allele carriers [2]. In elderly populations, some studies observed that non-carriers of the variant did not show a statistically significant reduction in vascular events when taking pravastatin [3]. Despite this, standard lipid-lowering guidelines still apply, and overall cardiovascular health should be managed through traditional risk factors.
Typical baseline risk of coronary heart disease; Standard clinical response to pravastatin therapy.
Sample genotype: AG (Heterozygous)
This genotype means carrying one copy of the G allele, which replaces tryptophan with arginine in the KIF6 protein. Prospective clinical trials have linked this carrier status to a higher baseline risk of myocardial infarction and coronary heart disease [1]. Fortunately, carriers of this variant also experience a much more pronounced reduction in cardiovascular events when treated with pravastatin [2]. In major clinical trials, pravastatin therapy significantly reduced fatal and non-fatal coronary events specifically in carriers of this variant [3]. While the baseline risk is elevated, the genetic susceptibility appears to be highly responsive to preventative statin therapy.
Elevated baseline risk of coronary heart disease; Enhanced clinical benefit from pravastatin therapy.
Sample genotype: GG (Homozygous)
This genotype means carrying two copies of the G allele, resulting in arginine at position 719 of both KIF6 proteins. This genetic profile is associated with an increased baseline risk of coronary heart disease and stroke [1]. Despite this higher baseline risk, clinical evidence shows that homozygous G carriers receive substantial cardiovascular protection from pravastatin therapy [2]. In trials of elderly patients, homozygous individuals on pravastatin experienced a significant reduction in major coronary events [3]. However, some research suggests that this genotype might show a slightly smaller reduction in LDL cholesterol levels when taking certain other statins, such as simvastatin or atorvastatin [4].
Elevated baseline risk of coronary heart disease and stroke; Enhanced clinical benefit from pravastatin therapy; Potentially altered lipid-lowering response to other statins.
Variants with shared genetic architecture
rs11556924 · ZC3HC1 Gene · Chr 7 · Heart Disease Risk
rs12740374 · CELSR2 Gene · Chr 1 · Heart Disease and Cholesterol
rs599839 · PSRC1 Gene · Chr 1 · Heart Disease Risk
Pharmacogenomics knowledge for personalized medicine.
KIF6 gene as a pharmacogenetic marker for lipid-lowering effect in statin treatment.
Content updated August 2026.
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