What you carry at this position in your DNA and what research says about it.
Blood Clotting Risk: 6/10 evidence, 14 publications.
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Sample genotype (not yours): C/C
Typical Blood Clotting Risk
Two copies of the common valine allele result in standard blood clotting rates and typical cardiovascular risk. Standard antiplatelet therapies like aspirin function normally in this genetic background.
What this genotype means: Standard blood clot structure; Typical baseline risk of cardiovascular events; Expected response to dual antiplatelet therapy.
Sample genotype (not yours): A/A
Lowest Risk of Blood Clots
Two copies of the leucine variant offer the strongest protection against deep vein thrombosis and heart attacks. However, this genotype is linked to a significantly reduced response to dual antiplatelet therapy.
What this genotype means: Lowest risk of venous thromboembolism; Highly permeable clot structure that dissolves easily; Significantly reduced efficacy of dual antiplatelet therapy.
Sample genotype (not yours): C/A
Lower Risk of Blood Clots
One copy of the leucine variant provides moderate protection against deep vein thrombosis and heart attacks. However, it may reduce the long-term efficacy of dual antiplatelet therapy.
What this genotype means: Moderately lower risk of deep vein thrombosis; Looser, more easily dissolved blood clots; Potential for reduced benefit from aspirin and clopidogrel.
Gene function and biological role
Gene Function: The F13A1 gene encodes the catalytic A subunit of coagulation factor XIII, a crucial enzyme in the final stages of the blood coagulation cascade [1]. Activated factor XIII stabilizes blood clots by covalently cross-linking fibrin chains, which increases the mechanical strength of the clot and protects it from premature degradation [1]. This process is essential for maintaining vascular integrity and preventing excessive bleeding after injury [2]. However, variations in this gene can alter the structure of the fibrin network, directly influencing an individual's susceptibility to both venous and arterial clotting events [2].
Variant Impact: The rs5985 variant, commonly known as Val34Leu or Val35Leu, represents a missense mutation in the F13A1 gene that substitutes the amino acid valine with leucine [1]. This specific change is located near the thrombin activation site, causing thrombin to cleave and activate factor XIII significantly faster than the reference version [1]. Paradoxically, this rapid activation leads to the formation of a looser, more permeable fibrin clot structure that is more easily broken down by the body's natural clot-dissolving mechanisms [2]. Consequently, this molecular alteration alters the physical properties of blood clots and modifies the risk of thromboembolic events [2].
Key Insight: Although the leucine variant causes blood to clot faster initially, it actually creates a looser clot structure that is easier for the body to dissolve, reducing overall clot risk.
Location: F13A1. Chromosome 6 · 6p25.1 · 6.3 Mb
Estimated prevalence by population
Global 61.9%; European 55.4%; African 66.5%; East Asian 99.5%; South Asian 78.0%; Americas 59.3%; Ashkenazi 69.0%; Finnish 63.1%; Middle Eastern 76.4%; Amish 39.5%.
Estimated CC genotype frequency.
Global 33.1%; European 38.1%; African 30.1%; East Asian 0.5%; South Asian 20.6%; Americas 35.4%; Ashkenazi 28.2%; Finnish 32.7%; Middle Eastern 22.0%; Amish 46.7%.
Estimated CA genotype frequency.
Global 4.9%; European 6.5%; African 3.4%; East Asian < 0.1%; South Asian 1.4%; Americas 5.3%; Ashkenazi 2.9%; Finnish 4.2%; Middle Eastern 1.6%; Amish 13.8%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Coagulation & Clotting
Venous Thromboembolism. Evidence: 3/10. Source: PMID 16740590. Typical Risk.
Blood Clotting Speed. Evidence: 6/10. Source: PMID 23381943. Typical Speed.
Heart Disease
Heart Attack. Evidence: 3/10. Source: PMID 16525568. Typical Risk.
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Antiplatelet Response. Evidence: 5/10. Source: PMID 24510702. Typical Response.
Showing effects for A/A genotype
Venous Thromboembolism. Evidence: 3/10. Source: PMID 16740590. Lowest Risk.
Blood Clotting Speed. Evidence: 6/10. Source: PMID 23381943. Fastest Clotting.
Heart Attack. Evidence: 3/10. Source: PMID 16525568. Lowest Risk.
Antiplatelet Response. Evidence: 5/10. Source: PMID 24510702. Lowest Efficacy.
Showing effects for C/A genotype
Venous Thromboembolism. Evidence: 3/10. Source: PMID 16740590. Lower Risk.
Blood Clotting Speed. Evidence: 6/10. Source: PMID 23381943. Faster Clotting.
Heart Attack. Evidence: 3/10. Source: PMID 16525568. Lower Risk.
Antiplatelet Response. Evidence: 5/10. Source: PMID 24510702. Reduced Efficacy.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having two copies of the reference valine allele means factor XIII is activated at a standard rate during the coagulation cascade [1]. This typical activation speed produces a standard fibrin clot structure with normal permeability and resistance to breakdown [1]. In the general population, this genotype represents the baseline risk for deep vein thrombosis, pulmonary embolism, and heart attacks [2]. Unlike carriers of the variant allele, individuals with this genotype do not experience a natural protective effect against these clotting disorders [2]. However, if cardiovascular disease develops, standard dual antiplatelet therapy with aspirin and clopidogrel performs as expected, showing typical efficacy and lower rates of recurrent events compared to variant carriers [3].
Standard blood clot structure; Typical baseline risk of cardiovascular events; Expected response to dual antiplatelet therapy.
Sample genotype: AA (Homozygous)
Carrying two copies of the leucine variant results in the fastest activation of factor XIII, leading to highly altered clot properties [1]. The resulting fibrin network is characterized by thicker fibers and larger pores, making the clots highly permeable and exceptionally easy for the body's natural systems to degrade [2]. Large-scale meta-analyses confirm that this genotype provides the strongest genetic protection against venous thromboembolism and heart attacks in the general population [2]. However, this altered clotting dynamic significantly impacts how the body responds to blood-thinning medications [3]. In patients undergoing dual antiplatelet therapy with aspirin and clopidogrel for coronary artery disease, this genotype is associated with a higher rate of recurrent cardiovascular events, suggesting standard antiplatelet protocols may be less effective [3].
Lowest risk of venous thromboembolism; Highly permeable clot structure that dissolves easily; Significantly reduced efficacy of dual antiplatelet therapy.
Sample genotype: CA (Heterozygous)
Carrying one copy of the leucine variant accelerates the activation of coagulation factor XIII by thrombin [1]. This rapid activation paradoxically alters the fibrin mesh, creating a looser and more permeable clot that the body can dissolve more easily [2]. Clinical studies and meta-analyses demonstrate that this altered clot structure provides moderate protection against venous thromboembolism and myocardial infarction in the general population [2]. Despite this natural cardiovascular benefit, the variant can interact unfavorably with certain medications [3]. Specifically, patients with established coronary artery disease who take aspirin and clopidogrel may experience a reduced therapeutic response, leading to a higher risk of recurrent events on these medications [3].
Moderately lower risk of deep vein thrombosis; Looser, more easily dissolved blood clots; Potential for reduced benefit from aspirin and clopidogrel.
Variants with shared genetic architecture
rs12041331 · PEAR1 Gene · Chr 1 · Blood Thinner Response
rs2066865 · FGG Gene · Chr 4 · Blood Clot Risk
rs710446 · KNG1 Gene · Chr 3 · Blood Clot Risk
Content updated August 2026.
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