F5 encodes coagulation factor V, a central regulator of hemostasis that serves as a critical cofactor for factor Xa in the prothrombinase complex, enabling prothrombin activation to thrombin. The protein is synthesized in the endoplasmic reticulum and transported via COPII-coated vesicles to the Golgi, ultimately secreted into plasma and stored in platelet alpha granules for hemostatic responses. Loss-of-function mutations cause factor V deficiency, a rare bleeding disorder. Conversely, the F5 Leiden variant (C506G polymorphism) confers activated protein C resistance, a major thrombophilia predisposing to venous thrombosis and recurrent pregnancy loss. This gain-of-function mutation prevents normal degradation of activated factor V, causing excessive thrombin generation. F5 polymorphisms have been investigated in obesity-related thrombotic risk, though associations remain unclear 1. Emerging evidence suggests F5 has roles beyond classical coagulation. Recent bioinformatics studies identified F5 as a diagnostic biomarker in severe asthma, associated with immune cell infiltration patterns 2. Additionally, F5 expression has been noted in cancer-associated fibroblast subpopulations within hepatocellular carcinoma tumors, potentially supporting cancer stem cell survival 3. Clinically, F5 testing is essential for thrombophilia screening, particularly in patients with unprovoked venous thromboembolism, recurrent miscarriage, or family histories of thrombosis. Anticoagulation management differs between factor V deficiency and thrombophilia, making accurate diagnosis critical for patient care.