What you carry at this position in your DNA and what research says about it.
Clotting and Heart Risk: 10/10 evidence, 35 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): A/A
Slightly Higher Heart Risk
Arterial health is slightly compromised, leading to a modest increase in the risk of coronary artery disease. Conversely, the risk of developing venous blood clots remains at the typical population baseline.
What this genotype means: Slightly increased risk of coronary artery disease; Typical risk of venous thromboembolism.
Sample genotype (not yours): A/G
Slightly Higher Clotting Risk
Carrying one copy of the G allele slightly elevates the risk of developing venous blood clots. This is accompanied by a corresponding decrease in the risk of coronary artery disease.
What this genotype means: Slightly increased risk of venous thromboembolism; Slightly reduced risk of coronary artery disease.
Sample genotype (not yours): G/G
Higher Clotting Risk but Heart Protection
Two copies of the G allele increase the risk of venous blood clots while providing significant protection against coronary artery disease. This genotype also offers substantial protection against severe malaria.
What this genotype means: Increased risk of venous thromboembolism; Reduced risk of coronary artery disease; Protection against severe malaria.
Gene function and biological role
Gene Function: The PROCR gene encodes the endothelial protein C receptor (EPCR), a key protein found on the surface of blood vessels [1]. EPCR plays a vital role in regulating blood clotting by binding to protein C and promoting its activation [1]. Once activated, protein C helps prevent excessive clot formation and dampens inflammatory responses [2]. Variations in this gene can alter how much EPCR remains bound to the cell surface versus how much is shed into the bloodstream [1]. This balance is critical for maintaining healthy blood flow and cardiovascular function [2].
Variant Impact: The rs867186 variant in the PROCR gene causes a missense mutation that swaps the amino acid serine for glycine at position 219 of the protein [1]. This structural change occurs in the transmembrane region of the receptor, making it more susceptible to being shed from the cell surface [1]. As a result, the variant allele is strongly associated with significantly higher levels of soluble EPCR in the plasma [1]. Because soluble EPCR can compete with cell-bound receptors, this shedding alters the activation of the anticoagulation pathway [3]. Consequently, this single nucleotide change influences both venous clotting risk and arterial cardiovascular health [3].
Key Insight: While the G allele increases the risk of deep vein blood clots, it simultaneously offers protection against coronary artery disease and severe malaria.
Location: PROCR. Chromosome 20 · 20q11.22 · 35.2 Mb
Origin Story: The G allele's ability to protect against severe malaria by preventing parasite-infected red blood cells from binding to blood vessels has likely contributed to its persistence in malaria-endemic regions.
Estimated prevalence by population
Global 81.6%; European 81.6%; African 82.4%; East Asian 85.3%; South Asian 70.7%; Americas 86.5%; Ashkenazi 77.0%; Finnish 75.0%; Middle Eastern 83.7%; Amish 83.8%.
Estimated AA genotype frequency.
Global 17.4%; European 17.4%; African 16.7%; East Asian 14.1%; South Asian 26.8%; Americas 13.1%; Ashkenazi 21.5%; Finnish 23.2%; Middle Eastern 15.6%; Amish 15.5%.
Estimated AG genotype frequency.
Global 1.0%; European 0.9%; African 0.8%; East Asian 0.6%; South Asian 2.5%; Americas 0.5%; Ashkenazi 1.5%; Finnish 1.8%; Middle Eastern 0.7%; Amish 0.7%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Coagulation & Clotting
Venous Thromboembolism. Evidence: 8/10. Source: PMID 38561338. Typical Risk.
Soluble EPCR Levels. Evidence: 8/10. Source: PMID 35870639. Typical Levels.
Heart Disease
Coronary Artery Disease. Evidence: 10/10. Source: PMID 29212778. Slightly Increased.
Immunity & Inflammation
Infection Susceptibility & Resistance
Severe Malaria. Evidence: 3/10. Source: PMID 24635948. Typical Risk.
Showing effects for A/G genotype
Venous Thromboembolism. Evidence: 8/10. Source: PMID 38561338. Slightly Increased.
Soluble EPCR Levels. Evidence: 8/10. Source: PMID 35870639. Elevated Levels.
Coronary Artery Disease. Evidence: 10/10. Source: PMID 29212778. Typical Risk.
Showing effects for G/G genotype
Venous Thromboembolism. Evidence: 8/10. Source: PMID 38561338. Increased Risk.
Soluble EPCR Levels. Evidence: 8/10. Source: PMID 35870639. High Levels.
Coronary Artery Disease. Evidence: 10/10. Source: PMID 29212778. Lower Risk.
Severe Malaria. Evidence: 3/10. Source: PMID 24635948. Reduced Risk.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Possessing two copies of the reference serine-encoding allele keeps the endothelial protein C receptor anchored to the blood vessel walls [1]. This results in typical levels of soluble EPCR in the bloodstream and standard activation of the anticoagulation pathway [1]. However, large-scale genetic studies show that this genotype is associated with a slightly higher risk of coronary artery disease and myocardial infarction compared to carriers of the G allele [2]. The precise mechanism linking the membrane-bound receptor to arterial plaque buildup is still being investigated, but it may involve localized inflammatory responses in the arterial wall [2]. On the positive side, this genotype does not carry the elevated risk of deep vein thrombosis or pulmonary embolism associated with the G allele [3]. It also provides typical susceptibility to severe malaria infections [4].
Slightly increased risk of coronary artery disease; Typical risk of venous thromboembolism.
Sample genotype: AG (Heterozygous)
A single copy of the G allele introduces the H3 haplotype, which is characterized by increased shedding of the endothelial protein C receptor into the bloodstream [1]. This leads to moderately elevated levels of soluble EPCR and circulating protein C [1]. Clinical data indicates that this alteration in the clotting cascade slightly increases the risk of venous thromboembolism, such as deep vein thrombosis [2]. Conversely, the presence of the G allele appears to be protective against arterial issues, resulting in a lower risk of coronary artery disease [3]. This trade-off highlights how a single genetic change can have opposing effects on different parts of the vascular system [3]. Susceptibility to severe malaria remains typical, as protection generally requires two copies of the protective allele [4].
Slightly increased risk of venous thromboembolism; Slightly reduced risk of coronary artery disease.
Sample genotype: GG (Homozygous)
Two copies of the G allele lead to the highest levels of soluble EPCR due to extensive shedding of the receptor from endothelial cells [1]. This pronounced shedding is associated with a clear increase in the risk of venous thromboembolism, as the loss of membrane-bound receptors impairs localized anticoagulation [2]. However, this same genetic profile is linked to a significantly lower risk of coronary artery disease and myocardial infarction [3]. Furthermore, the high levels of soluble EPCR act as a decoy that prevents malaria-infected red blood cells from adhering to blood vessels, offering strong protection against severe malaria [4]. This dual nature makes the G/G genotype a classic example of genetic trade-offs in vascular health [3].
Increased risk of venous thromboembolism; Reduced risk of coronary artery disease; Protection against severe malaria.
Variants with shared genetic architecture
rs2066865 · FGG Gene · Chr 4 · Blood Clot Risk
rs5498 · ICAM1 Gene · Chr 19 · Heart Disease Risk
rs1801020 · F12 Gene · Chr 5 · Blood Clotting and Heart Health
Genetic associations of protein-coding variants in venous thromboembolism.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com