What you carry at this position in your DNA and what research says about it.
Blood Thinner Response: 10/10 evidence, 25 publications.
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Sample genotype (not yours): G/G
Typical Bleeding and Cardiovascular Risk on Therapy
Platelets exhibit typical stickiness and aggregation patterns. This genotype is associated with a standard response to antiplatelet medications like aspirin and clopidogrel.
What this genotype means: Typical platelet aggregation; Standard bleeding risk on blood thinners; Lower risk of cardiovascular events on therapy compared to A carriers.
Sample genotype (not yours): A/A
Highest Bleeding and Cardiovascular Risk on Therapy
Platelets have the lowest stickiness, resulting in the highest risk of bleeding on blood thinners. This genotype is also linked to a higher rate of cardiovascular complications during treatment.
What this genotype means: Lowest platelet aggregation; Highest risk of bleeding on antiplatelet drugs; Significantly increased risk of cardiovascular events under therapy.
Sample genotype (not yours): G/A
Increased Bleeding and Cardiovascular Risk on Therapy
Platelets are less sticky, which can reduce clotting but increases the risk of bleeding. There is also an elevated risk of cardiovascular events when taking certain blood thinners.
What this genotype means: Reduced platelet aggregation; Elevated risk of bleeding on antiplatelet drugs; Increased risk of cardiovascular events under therapy.
Gene function and biological role
Gene Function: The PEAR1 gene encodes the platelet endothelial aggregation receptor 1 protein, a critical receptor found on the surface of platelets and endothelial cells. This protein plays a vital role in regulating platelet-to-platelet contact and the overall aggregation process during blood clotting. By modulating these pathways, the gene helps maintain a delicate balance between preventing excessive bleeding and avoiding unwanted arterial clots. Genetic variations within this gene can significantly alter how platelets respond to physiological triggers and antiplatelet medications. Understanding these variations helps clarify individual differences in cardiovascular health and drug efficacy.
Variant Impact: The rs12041331 variant is located within the first intron of the PEAR1 gene and acts as a major genetic modifier of platelet function. The presence of the minor A allele is associated with reduced PEAR1 protein expression on the surface of platelets. This reduction in protein levels leads to suppressed platelet aggregation in response to common clotting stimulants. Consequently, this single nucleotide change alters how the blood clots and how it responds to antiplatelet therapies. It represents one of the most widely studied genetic factors in personalized cardiovascular medicine.
Key Insight: The A allele reduces platelet stickiness, which makes blood thinners more effective at preventing aggregation but paradoxically increases the risk of both bleeding and certain cardiovascular events in clinical studies.
Location: PEAR1. Chromosome 1 · 1q23.1 · 156.9 Mb
Estimated prevalence by population
Global 66.2%; European 83.0%; African 39.1%; East Asian 32.5%; South Asian 44.2%; Americas 63.4%; Ashkenazi 77.4%; Finnish 89.6%; Middle Eastern 66.6%; Amish 82.8%.
Estimated GG genotype frequency.
Global 28.1%; European 16.2%; African 46.8%; East Asian 49.0%; South Asian 44.6%; Americas 32.4%; Ashkenazi 21.2%; Finnish 10.1%; Middle Eastern 30.0%; Amish 16.4%.
Estimated GA genotype frequency.
Global 5.7%; European 0.8%; African 14.0%; East Asian 18.5%; South Asian 11.2%; Americas 4.1%; Ashkenazi 1.4%; Finnish 0.3%; Middle Eastern 3.4%; Amish 0.8%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Bleeding Risk on Medication. Evidence: 5/10. Source: PMID 37891772. Typical Risk.
Cardiovascular & Metabolic
Heart Disease
Cardiovascular Events. Evidence: 5/10. Source: PMID 23392654. Typical Risk.
Coagulation & Clotting
Platelet Aggregation. Evidence: 10/10. Source: PMID 21791418. Typical Aggregation.
Blood Cell & Iron Traits
Mean Platelet Volume. Evidence: 10/10. Source: PMID 27863252. Slightly Higher.
Platelet Count. Evidence: 10/10. Source: PMID 29403010. Typical.
Showing effects for A/A genotype
Bleeding Risk on Medication. Evidence: 5/10. Source: PMID 37891772. Highest Risk.
Cardiovascular Events. Evidence: 5/10. Source: PMID 23392654. Highest Risk.
Platelet Aggregation. Evidence: 10/10. Source: PMID 21791418. Lowest Aggregation.
Mean Platelet Volume. Evidence: 10/10. Source: PMID 27863252. Slightly Lower.
Platelet Count. Evidence: 10/10. Source: PMID 29403010. Higher.
Showing effects for G/A genotype
Bleeding Risk on Medication. Evidence: 5/10. Source: PMID 37891772. Increased Risk.
Cardiovascular Events. Evidence: 5/10. Source: PMID 23392654. Increased Risk.
Platelet Aggregation. Evidence: 10/10. Source: PMID 21791418. Reduced Aggregation.
Mean Platelet Volume. Evidence: 10/10. Source: PMID 27863252. Typical.
Platelet Count. Evidence: 10/10. Source: PMID 29403010. Slightly Higher.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Having two copies of the G allele is associated with typical levels of PEAR1 protein expression on platelets. Platelets maintain standard aggregability, meaning they clump together normally to form clots when needed. When taking antiplatelet therapies such as aspirin or clopidogrel, individuals with this genotype experience a typical risk of bleeding complications. They also show a lower rate of adverse cardiovascular events and myocardial infarction under these therapies compared to carriers of the A allele. This genotype represents the most common genetic profile globally, providing a baseline standard of care. Clinical trials suggest that standard antiplatelet dosing strategies perform as expected in this group.
Typical platelet aggregation; Standard bleeding risk on blood thinners; Lower risk of cardiovascular events on therapy compared to A carriers.
Sample genotype: AA (Homozygous)
Carrying two copies of the A allele results in the lowest levels of PEAR1 protein expression and the most suppressed platelet aggregation. This highly suppressed state significantly elevates the risk of bleeding complications when taking antiplatelet medications like aspirin, clopidogrel, or ticagrelor. Paradoxically, clinical data shows that individuals with this genotype have up to a three-fold increase in short-term major adverse cardiovascular events after coronary stenting. This suggests that the profound reduction in platelet stickiness does not translate to clinical protection and instead correlates with poorer cardiovascular outcomes on dual therapy. This genetic profile represents a critical factor in evaluating personal response to blood thinners.
Lowest platelet aggregation; Highest risk of bleeding on antiplatelet drugs; Significantly increased risk of cardiovascular events under therapy.
Sample genotype: GA (Heterozygous)
Carrying one copy of the A allele leads to a moderate reduction in PEAR1 protein expression. This reduction suppresses platelet aggregation, making the blood less prone to clumping. While this can enhance the pharmacological response to antiplatelet drugs, it also significantly increases the risk of bleeding events during treatment. Paradoxically, clinical studies have observed that carriers of this variant undergoing coronary procedures have an increased risk of major adverse cardiovascular events. This dual effect suggests that while platelets are less sticky, the overall vascular response under therapy is altered. The presence of this allele may influence clinical decisions regarding the choice and monitoring of antiplatelet regimens.
Reduced platelet aggregation; Elevated risk of bleeding on antiplatelet drugs; Increased risk of cardiovascular events under therapy.
Variants with shared genetic architecture
rs12566888 · PEAR1 Gene · Chr 1 · Blood Clot Risk
rs6065 · GP1BA Gene · Chr 17 · Platelet Function and Stroke
rs75326924 · CD36 Gene · Chr 7 · Platelet CD36 Deficiency
Content updated August 2026.
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