What you carry at this position in your DNA and what research says about it.
Venous Thrombosis Risk: 10/10 evidence, 24 publications.
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Sample genotype (not yours): G/G
Lowest Risk of Venous Blood Clots
Carrying two copies of the protective G allele is associated with the lowest platelet reactivity and lowest glycoprotein VI levels. This provides the strongest genetic protection against deep vein thrombosis.
What this genotype means: Reduced platelet reactivity; Lower glycoprotein VI receptor expression; Significantly lower risk of deep vein thrombosis.
Sample genotype (not yours): A/A
Higher Risk of Venous Blood Clots
Having two copies of the A allele is associated with higher platelet reactivity and elevated levels of glycoprotein VI. This increases the likelihood of developing deep vein thrombosis or other venous blood clots.
What this genotype means: Increased platelet reactivity; Higher glycoprotein VI receptor expression; Elevated risk of deep vein thrombosis.
Sample genotype (not yours): G/A
Lower Risk of Venous Blood Clots
Carrying one copy of the protective G allele is linked to reduced platelet reactivity and lower glycoprotein VI levels. This helps lower the overall risk of developing deep vein thrombosis.
What this genotype means: Moderately reduced platelet reactivity; Intermediate glycoprotein VI receptor expression; Lower risk of deep vein thrombosis.
Gene function and biological role
Gene Function: The GP6 gene encodes glycoprotein VI, a crucial receptor found on the surface of blood platelets [1]. This receptor plays a central role in blood clotting by binding to collagen exposed when blood vessels are damaged [1]. Once bound, it triggers platelet activation and aggregation to form a plug and stop bleeding [1]. Variations in this gene can alter the density of these receptors on platelets, directly influencing how easily blood clots [2]. Consequently, GP6 is a key focus in research on both bleeding disorders and cardiovascular clotting risks [2].
Variant Impact: The rs1613662 variant is a missense change in the GP6 gene that substitutes the amino acid proline with serine at position 219 of the glycoprotein VI protein. This structural alteration directly impacts the stability and expression levels of the receptor on the platelet surface [1]. The G allele (encoding proline) leads to lower receptor density, whereas the A allele (encoding serine) results in higher receptor density [1]. Because receptor density dictates how sensitively platelets react to collagen, this single change influences overall blood clotting tendency [2]. Research has heavily focused on how this variation affects susceptibility to abnormal blood clots in the veins [2].
Key Insight: A single amino acid change in the GP6 receptor acts like a dimmer switch for platelet sensitivity, directly altering how aggressively your blood clots in response to vessel injury.
Location: GP6. Chromosome 19 · 19q13.42 · 55.0 Mb
Estimated prevalence by population
Global 3.0%; European 2.4%; African 5.1%; East Asian 0.1%; South Asian 4.6%; Americas 1.3%; Ashkenazi 4.2%; Finnish 1.2%; Middle Eastern 2.2%; Amish 5.3%.
Estimated GG genotype frequency.
Global 27.2%; European 26.1%; African 35.0%; East Asian 4.7%; South Asian 33.6%; Americas 20.0%; Ashkenazi 32.6%; Finnish 19.6%; Middle Eastern 25.5%; Amish 35.4%.
Estimated GA genotype frequency.
Global 69.8%; European 71.5%; African 59.8%; East Asian 95.2%; South Asian 61.8%; Americas 78.7%; Ashkenazi 63.2%; Finnish 79.2%; Middle Eastern 72.3%; Amish 59.3%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Coagulation & Clotting
Venous Thromboembolism. Evidence: 4/10. Source: PMID 20124536. ~34% Lower Risk.
Platelet Reactivity. Evidence: 6/10. Source: PMID 34581777. Lowest Reactivity.
Platelet Glycoprotein VI. Evidence: 8/10. Source: PMID 36168886. Lowest Levels.
Blood Cell & Iron Traits
Mean Platelet Volume. Evidence: 10/10. Source: PMID 27863252. Lowest Volume.
Lifestyle, Fitness & Aging
Aging & Longevity
Mitochondrial DNA Copy Number. Evidence: 8/10. Source: PMID 33385171. Highest Copy Number.
Showing effects for A/A genotype
Venous Thromboembolism. Evidence: 4/10. Source: PMID 20124536. ~1.15x Elevated Risk.
Platelet Reactivity. Evidence: 6/10. Source: PMID 34581777. Highest Reactivity.
Platelet Glycoprotein VI. Evidence: 8/10. Source: PMID 36168886. Highest Levels.
Mean Platelet Volume. Evidence: 10/10. Source: PMID 27863252. Highest Volume.
Mitochondrial DNA Copy Number. Evidence: 8/10. Source: PMID 33385171. Lowest Copy Number.
Showing effects for G/A genotype
Venous Thromboembolism. Evidence: 4/10. Source: PMID 20124536. ~20% Lower Risk.
Platelet Reactivity. Evidence: 6/10. Source: PMID 34581777. Lower Reactivity.
Platelet Glycoprotein VI. Evidence: 8/10. Source: PMID 36168886. Lower Levels.
Mean Platelet Volume. Evidence: 10/10. Source: PMID 27863252. Lower Volume.
Mitochondrial DNA Copy Number. Evidence: 8/10. Source: PMID 33385171. Higher Copy Number.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Platelets with this genotype express the lowest levels of glycoprotein VI receptors, significantly reducing their ability to adhere to collagen [1]. This leads to a marked decrease in platelet reactivity and smaller mean platelet volumes [2]. Clinical studies demonstrate that this genotype offers substantial protection against abnormal venous clotting [3]. Individuals with two copies of the G allele have an estimated 34% lower risk of venous thromboembolism compared to those with the common A/A genotype [3]. This natural reduction in clotting tendency does not trigger clinical bleeding disorders, as confirmed by ClinVar. It represents a highly favorable genetic profile for avoiding deep vein thrombosis and pulmonary embolism.
Reduced platelet reactivity; Lower glycoprotein VI receptor expression; Significantly lower risk of deep vein thrombosis.
Sample genotype: AA (Homozygous)
Platelets with this genotype express a higher density of glycoprotein VI receptors on their surface, making them more sensitive to collagen binding [1]. This heightened sensitivity leads to increased platelet reactivity and larger mean platelet volumes [2]. Clinical studies have shown that this hyper-reactive state translates to a modest but significant increase in the risk of venous thromboembolism [3]. Specifically, carrying two copies of the A allele is associated with an approximate 15% to 20% higher risk of deep vein thrombosis compared to carrying the protective G allele [3]. Despite this elevated clotting risk, ClinVar assessments confirm that this common genotype does not cause platelet-type bleeding disorders. Maintaining a healthy cardiovascular lifestyle is the standard approach to managing this common genetic baseline.
Increased platelet reactivity; Higher glycoprotein VI receptor expression; Elevated risk of deep vein thrombosis.
Sample genotype: GA (Heterozygous)
Having one copy of the G allele introduces a proline residue that reduces the density of glycoprotein VI receptors on platelets [1]. This reduction tempers platelet reactivity and decreases the overall sensitivity of the clotting cascade [1]. Research indicates that individuals with this heterozygous genotype enjoy a lower risk of venous thromboembolism compared to those with the typical A/A genotype [2]. Specifically, carrying at least one G allele is associated with an approximate 20% reduction in the risk of deep vein thrombosis [2]. Additionally, this genotype is linked to smaller mean platelet volumes and lower overall platelet activation [3]. These biological changes provide a natural, mild protective effect against abnormal clot formation in the veins.
Moderately reduced platelet reactivity; Intermediate glycoprotein VI receptor expression; Lower risk of deep vein thrombosis.
Variants with shared genetic architecture
rs1671152 · GP6 Gene · Chr 19 · Platelet Aggregation
rs1654425 · GP6 Gene · Chr 19 · Blood Clot Risk
rs1354034 · ARHGEF3 Gene · Chr 3 · Platelet Count and Size
Updated analysis of gene variants associated with deep vein thrombosis.
The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.
Content updated August 2026.
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