What you carry at this position in your DNA and what research says about it.
Blood Clot Risk: 10/10 evidence, 22 publications.
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Sample genotype (not yours): G/G
Typical Blood Clot Risk
Typical levels of fibrinogen gamma-prime and a standard baseline risk for blood clots.
What this genotype means: Typical risk of deep vein thrombosis; Typical risk of pulmonary embolism.
Sample genotype (not yours): A/A
Moderately Increased Blood Clot Risk
Two copies of the A allele, which is linked to a moderately higher risk of blood clots and pulmonary embolism.
What this genotype means: Moderately higher risk of deep vein thrombosis; Moderately higher risk of pulmonary embolism.
Sample genotype (not yours): G/A
Slightly Increased Blood Clot Risk
One copy of the A allele, which is associated with a slightly higher risk of developing blood clots.
What this genotype means: Slightly higher risk of deep vein thrombosis; Slightly higher risk of pulmonary embolism.
Gene function and biological role
Gene Function: The FGG gene encodes the gamma chain of fibrinogen, a key glycoprotein essential for blood clot formation [1]. Fibrinogen is converted into fibrin during blood coagulation, forming a mesh that stabilizes clots [1]. Variations in this gene can alter the ratio of different fibrinogen isoforms, specifically reducing the protective gamma-prime isoform [1]. This reduction in gamma-prime fibrinogen can lead to a prothrombotic state, making clots more resistant to breakdown [1].
Variant Impact: Altering the splicing or expression of the gamma-prime isoform, the rs2066865 variant leads to decreased levels of this protective fibrinogen variant [1]. This change is strongly associated with an increased susceptibility to venous thromboembolism and deep vein thrombosis [2]. Although it increases clotting risk, ClinVar assessments confirm it is benign for congenital afibrinogenemia, meaning it does not cause a complete lack of fibrinogen. The variant is relatively common, with the minor A allele present in about 26 percent of the global population.
Key Insight: Carrying the A allele reduces the levels of a specific protective form of fibrinogen, making blood clots more likely to form and harder to break down.
Location: FGG. Chromosome 4 · 4q32.1 · 154.6 Mb
Estimated prevalence by population
Global 54.1%; European 57.5%; African 48.7%; East Asian 30.7%; South Asian 49.8%; Americas 60.5%; Ashkenazi 73.4%; Finnish 49.7%; Middle Eastern 70.6%; Amish 55.5%.
Estimated GG genotype frequency.
Global 38.6%; European 36.7%; African 42.2%; East Asian 49.4%; South Asian 41.5%; Americas 34.5%; Ashkenazi 24.6%; Finnish 41.6%; Middle Eastern 26.9%; Amish 38.0%.
Estimated GA genotype frequency.
Global 7.3%; European 5.8%; African 9.1%; East Asian 19.9%; South Asian 8.6%; Americas 4.9%; Ashkenazi 2.1%; Finnish 8.7%; Middle Eastern 2.6%; Amish 6.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Coagulation & Clotting
Venous Thromboembolism. Evidence: 10/10. Source: PMID 25772935. Typical Risk.
Pulmonary Embolism. Evidence: 8/10. Source: PMID 37076872. Typical Risk.
Thrombophlebitis. Evidence: 8/10. Source: PMID 39024449. Typical Risk.
Heart Disease
Heart Disease. Evidence: 8/10. Source: PMID 39024449. Typical Risk.
Showing effects for A/A genotype
Venous Thromboembolism. Evidence: 10/10. Source: PMID 25772935. ~1.6x Increased Risk.
Pulmonary Embolism. Evidence: 8/10. Source: PMID 37076872. ~1.37x Increased Risk.
Thrombophlebitis. Evidence: 8/10. Source: PMID 39024449. Increased Risk.
Heart Disease. Evidence: 8/10. Source: PMID 39024449. Increased Risk.
Showing effects for G/A genotype
Venous Thromboembolism. Evidence: 10/10. Source: PMID 25772935. Slightly Increased.
Pulmonary Embolism. Evidence: 8/10. Source: PMID 37076872. Slightly Increased.
Thrombophlebitis. Evidence: 8/10. Source: PMID 39024449. Slightly Increased.
Heart Disease. Evidence: 8/10. Source: PMID 39024449. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Fibrinogen levels and clotting risks are typical for those carrying two copies of the G allele [1]. Standard baseline risks for deep vein thrombosis and pulmonary embolism apply to this genetic profile [2]. Research indicates that the elevated risk of clotting associated with the A allele is absent here [3]. This common genetic signature is found in about 73 percent of the global population. Maintaining a healthy lifestyle, staying active, and avoiding prolonged immobility remain the best ways to support cardiovascular health. Regular physical activity and hydration help maintain optimal blood flow. Standard medical guidelines do not recommend any special precautions for this typical profile.
Typical risk of deep vein thrombosis; Typical risk of pulmonary embolism.
Sample genotype: AA (Homozygous)
Two copies of the A allele significantly reduce the levels of the protective fibrinogen gamma-prime isoform in the blood [1]. This reduction leads to a prothrombotic state, where blood clots form more easily and are more resistant to natural breakdown [1]. Clinical studies have shown a moderately increased risk of venous thromboembolism, with some studies estimating a 1.6-fold to 1.7-fold higher risk compared to non-carriers. The risk of pulmonary embolism, a serious condition where a clot travels to the lungs, is also elevated [2]. This genetic predisposition is particularly relevant during periods of high risk, such as major surgery, active cancer, or prolonged immobility. While this profile increases susceptibility, it is not a guarantee that a clot will form, and preventive measures can significantly mitigate the risk [3]. Discussing these findings with a physician before major medical procedures can help tailor appropriate clot-prevention strategies.
Moderately higher risk of deep vein thrombosis; Moderately higher risk of pulmonary embolism.
Sample genotype: GA (Heterozygous)
A single copy of the A allele is associated with a slight reduction in protective fibrinogen gamma-prime levels [1]. This reduction can make blood clots slightly more likely to form in the veins, a condition known as venous thromboembolism [2]. Large-scale genetic studies have linked this genetic profile to a modest increase in the risk of deep vein thrombosis and pulmonary embolism. The risk is further influenced by lifestyle factors such as long-distance travel, surgery, or prolonged immobility [3]. Knowing this status can help you and your healthcare provider make informed decisions during high-risk periods like surgeries or long flights [3]. Standard preventive measures like compression stockings or movement during travel are often recommended. Overall cardiovascular health can be supported by staying active and hydrated.
Slightly higher risk of deep vein thrombosis; Slightly higher risk of pulmonary embolism.
Variants with shared genetic architecture
rs10886430 · GRK5 Gene · Chr 10 · Blood Clot Risk
rs12445050 · PLCG2 Gene · Chr 16 · Blood Clot Risk
rs6025 · F5 Gene · Chr 1 · Blood Clot Risk
The fibrinogen gamma (FGG) 10034C>T polymorphism is associated with venous thrombosis.
Content updated August 2026.
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