What you carry at this position in your DNA and what research says about it.
Heart Attack Risk: 7/10 evidence, 31 publications.
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Sample genotype (not yours): T/T
Typical Heart Attack and Clotting Risk
Standard platelet function and typical response to aspirin. No elevated risk of early-onset heart attacks from this genetic marker.
What this genotype means: Typical platelet clotting activity; Standard response to aspirin therapy.
Sample genotype (not yours): C/C
Higher Heart Attack Risk and Aspirin Resistance
Higher risk of early-onset heart attacks and reduced sensitivity to aspirin's blood-thinning benefits.
What this genotype means: Elevated risk of early-onset heart attacks; Reduced effectiveness of aspirin for clot prevention.
Sample genotype (not yours): T/C
Increased Heart Attack Risk and Aspirin Resistance
Slightly higher risk of early-onset heart attacks and reduced sensitivity to aspirin's blood-thinning benefits.
Gene function and biological role
Gene Function: The ITGB3 gene encodes integrin subunit beta 3, a key protein component of the platelet glycoprotein IIb/IIIa receptor complex [1]. This receptor plays a vital role in blood clotting by binding to fibrinogen and promoting platelet aggregation [2]. Proper functioning of this gene is essential for preventing excessive bleeding while avoiding unwanted clot formation [3]. Variations in this gene can alter the receptor's structure, affecting how platelets respond to clotting signals and medications [1].
Variant Impact: The rs5918 variant is a missense mutation in the ITGB3 gene that changes the amino acid leucine to proline at position 59 of the protein, historically referred to as position 33 [1]. This change defines the difference between the common PlA1 (leucine) and the minor PlA2 (proline) platelet antigens [4]. The structural alteration increases the binding affinity of platelets to fibrinogen, making them more hyperreactive [2]. This hyperreactivity can lead to a higher tendency for blood clots to form in arteries, potentially increasing cardiovascular risks [5].
Key Insight: The PlA2 variant of this gene can make platelets hyperreactive, meaning they stick together and form clots more easily. While this variant increases heart attack risk and reduces aspirin's effectiveness, it has been linked to a lower risk of non-Hodgkin lymphoma.
Location: ITGB3. Chromosome 17 · 17q21.32 · 47.3 Mb
Estimated prevalence by population
Global 76.2%; European 71.2%; African 80.0%; East Asian 98.7%; South Asian 81.2%; Americas 80.6%; Ashkenazi 73.3%; Finnish 75.1%; Middle Eastern 73.5%; Amish 72.4%.
Estimated TT genotype frequency.
Global 22.0%; European 26.3%; African 18.8%; East Asian 1.3%; South Asian 17.8%; Americas 18.4%; Ashkenazi 24.6%; Finnish 23.1%; Middle Eastern 24.5%; Amish 25.4%.
Estimated TC genotype frequency.
Global 1.7%; European 2.4%; African 1.1%; East Asian < 0.1%; South Asian 1.0%; Americas 1.0%; Ashkenazi 2.1%; Finnish 1.8%; Middle Eastern 2.0%; Amish 2.2%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Heart Disease
Heart Attack. Evidence: 4/10. Source: PMID 8598867. Typical Risk.
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Aspirin Resistance. Evidence: 5/10. Source: PMID 11723016. Typical Response.
Cancer & Oncology
Blood Cancers
Non-Hodgkin Lymphoma. Evidence: 6/10. Typical Risk.
Nutrition & Metabolism
Blood Chemistry & Metabolites
Serum Globulin Levels. Evidence: 7/10. Source: PMID 33462484. Higher Levels.
Showing effects for C/C genotype
Heart Attack. Evidence: 4/10. Source: PMID 8598867. Increased Risk.
Aspirin Resistance. Evidence: 5/10. Source: PMID 11723016. Reduced Response.
Non-Hodgkin Lymphoma. Evidence: 6/10. Lower Risk.
Serum Globulin Levels. Evidence: 7/10. Source: PMID 33462484. Lower Levels.
Showing effects for T/C genotype
Serum Globulin Levels. Evidence: 7/10. Source: PMID 33462484. Intermediate.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Leucine-encoding alleles at this position represent the most common genetic profile [1]. Platelets function normally, showing typical binding affinity to fibrinogen and standard aggregation responses [2]. There is no genetically elevated risk of premature myocardial infarction or coronary artery disease associated with this site [3]. Furthermore, when aspirin is prescribed for cardiovascular protection, it typically works as expected to inhibit platelet clotting [2]. This profile serves as the baseline comparison for studies on platelet reactivity and cardiovascular risk [1].
Typical platelet clotting activity; Standard response to aspirin therapy.
Sample genotype: CC (Homozygous)
Two copies of the proline-encoding C allele (the PlA2 variant) significantly alter the glycoprotein IIIa receptor on the surface of platelets [1]. This homozygous profile is associated with enhanced platelet aggregation and a stronger tendency to form arterial clots [2]. Research indicates a significantly increased risk of premature coronary artery disease and myocardial infarction [3]. Furthermore, the anti-clotting effects of aspirin are often diminished in this genotype, which may lead to aspirin resistance [2]. Interestingly, this genetic variant has also been associated with a reduced risk of developing non-Hodgkin lymphoma [1].
Elevated risk of early-onset heart attacks; Reduced effectiveness of aspirin for clot prevention.
Sample genotype: TC (Heterozygous)
A single proline-encoding C allele (also known as the PlA2 variant) alters the structure of the glycoprotein IIIa receptor on platelets [1]. This structural change increases the binding affinity of platelets to fibrinogen, making them more prone to aggregation and clotting [2]. Clinical studies have linked this variant to an elevated risk of premature myocardial infarction and coronary artery disease [3]. Additionally, individuals with this genotype may experience reduced platelet inhibition when taking aspirin, potentially lowering its effectiveness in preventing clots [2]. However, some research suggests a potential protective effect against developing non-Hodgkin lymphoma [1].
Variants with shared genetic architecture
rs10886430 · GRK5 Gene · Chr 10 · Blood Clot Risk
rs12445050 · PLCG2 Gene · Chr 16 · Blood Clot Risk
rs1654425 · GP6 Gene · Chr 19 · Blood Clot Risk
A monoclonal antibody (SZ21) specific for platelet GPIIIa distinguishes P1A1 from P1A2.
Content updated August 2026.
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