What you carry at this position in your DNA and what research says about it.
Platelet Aggregation: 10/10 evidence, 8 publications.
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Sample genotype (not yours): T/T
Higher Platelet Aggregation and Clotting Tendency
Two copies of the T allele are associated with more sensitive platelets that clump together more easily. This can lead to a higher tendency for blood clotting.
What this genotype means: Increased platelet aggregation; Higher tendency for blood clotting; Linked to sticky platelet syndrome.
Sample genotype (not yours): G/G
Typical Platelet Aggregation and Clotting Tendency
Two copies of the G allele are associated with normal platelet aggregation. This represents a typical, healthy baseline for blood clotting.
What this genotype means: Typical platelet aggregation; Normal blood clotting baseline; Classified as benign by ClinVar.
Sample genotype (not yours): T/G
Slightly Higher Platelet Aggregation and Clotting Tendency
Carrying one copy of the T allele is associated with moderately increased platelet aggregation. This can lead to a slightly higher tendency for blood clotting.
What this genotype means: Moderately increased platelet aggregation; Slightly higher clotting tendency.
Gene function and biological role
Gene Function: Glycoprotein VI, encoded by the GP6 gene, is a vital receptor found on the surface of blood platelets. It plays a central role in the body's clotting response by binding directly to collagen exposed at sites of blood vessel injury [1]. This interaction triggers platelet activation and aggregation, which are essential for stopping bleeding [1]. Genetic variations in this gene can alter how sensitively platelets react to these signals [2]. This can influence an individual's overall tendency to form blood clots [2].
Variant Impact: The rs1671152 variant is a missense mutation in the GP6 gene that changes the amino acid at position 322 from asparagine to histidine. This structural alteration occurs in the extracellular domain of the glycoprotein VI receptor, directly affecting its signaling capacity. Research indicates that this change modifies how platelets respond to collagen stimulation [1]. The variation is a key genetic determinant of individual differences in platelet aggregation [2].
Key Insight: The minor T allele is linked to significantly higher platelet aggregation, which can make platelets stickier and increase clotting tendencies.
Location: GP6. Chromosome 19 · 19q13.42 · 55.0 Mb
Estimated prevalence by population
Global 4.1%; European 2.2%; African 9.3%; East Asian 0.1%; South Asian 4.5%; Americas 1.3%; Ashkenazi 3.8%; Finnish 1.2%; Middle Eastern 2.4%; Amish 5.4%.
Estimated TT genotype frequency.
Global 28.8%; European 25.4%; African 42.4%; East Asian 4.8%; South Asian 33.5%; Americas 20.0%; Ashkenazi 31.3%; Finnish 19.5%; Middle Eastern 26.2%; Amish 35.6%.
Estimated TG genotype frequency.
Global 67.1%; European 72.4%; African 48.3%; East Asian 95.1%; South Asian 62.0%; Americas 78.8%; Ashkenazi 64.9%; Finnish 79.3%; Middle Eastern 71.4%; Amish 59.0%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Coagulation & Clotting
Platelet Aggregation. Evidence: 8/10. Source: PMID 20526338. Increased.
Blood Cell & Iron Traits
Platelet Count. Evidence: 10/10. Source: PMID 32888494. Not established.
Reticulocyte Count. Evidence: 7/10. Source: PMID 27863252. Typical.
Immunity & Inflammation
Autoimmune Diseases
Rheumatoid Arthritis. Evidence: 3/10. Source: PMID 23739280. No Association.
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Aspirin Response. Evidence: 3/10. Source: PMID 21854539. Slightly Altered.
Showing effects for G/G genotype
Platelet Aggregation. Evidence: 8/10. Source: PMID 20526338. Typical.
Reticulocyte Count. Evidence: 7/10. Source: PMID 27863252. Increased.
Aspirin Response. Evidence: 3/10. Source: PMID 21854539. Typical.
Showing effects for T/G genotype
Platelet Aggregation. Evidence: 8/10. Source: PMID 20526338. Slightly Increased.
Reticulocyte Count. Evidence: 7/10. Source: PMID 27863252. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Having two copies of the T allele at this locus is associated with significantly increased platelet aggregation in response to collagen [1]. This hyper-reactivity means that platelets clump together more readily, which can increase the risk of abnormal blood clots [1]. In some clinical studies, this increased sensitivity has been linked to conditions like sticky platelet syndrome [2]. However, this variant does not appear to have any significant association with susceptibility to rheumatoid arthritis [3]. It also has a weak nominal association with platelet reactivity during aspirin therapy, though the clinical impact of this is minor [4]. Overall, this genotype represents a higher-than-average clotting tendency.
Increased platelet aggregation; Higher tendency for blood clotting; Linked to sticky platelet syndrome.
Sample genotype: GG (Homozygous)
Having two copies of the G allele is the most common genetic profile globally and is associated with typical platelet aggregation [1]. Platelets react normally to collagen stimulation, maintaining a healthy balance between clotting and bleeding [1]. ClinVar assessments classify this common variant as benign, confirming it does not cause platelet-type bleeding disorders [2]. Furthermore, genetic studies have shown that this genotype is not associated with an increased risk or severity of rheumatoid arthritis [3]. It also represents a standard response to aspirin therapy, with no significant deviation in platelet reactivity [4]. This genotype provides a stable, typical baseline for cardiovascular and clotting health.
Typical platelet aggregation; Normal blood clotting baseline; Classified as benign by ClinVar.
Sample genotype: TG (Heterozygous)
Carrying one copy of the T allele is associated with an intermediate increase in platelet aggregation compared to the typical genotype [1]. Platelets with this genetic makeup tend to react more sensitively to collagen, making them slightly more prone to clumping [1]. This moderate increase in reactivity is part of the genetic spectrum of platelet function variation [2]. Studies examining this variant in the context of rheumatoid arthritis have found no significant association, suggesting it does not affect joint inflammation [3]. It may also play a minor role in how platelets respond to aspirin therapy, though the effect is subtle [4]. Individuals with this genotype have a slightly elevated clotting tendency compared to those with the common G/G genotype.
Moderately increased platelet aggregation; Slightly higher clotting tendency.
Variants with shared genetic architecture
rs1613662 · GP6 Gene · Chr 19 · Venous Thrombosis Risk
rs1654425 · GP6 Gene · Chr 19 · Blood Clot Risk
rs1354034 · ARHGEF3 Gene · Chr 3 · Platelet Count and Size
Association study of the platelet collagen receptor glycoprotein VI gene with rheumatoid arthritis.
Content updated August 2026.
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