F3 encodes tissue factor (TF), the primary initiator of blood coagulation through formation of a TF:VIIa complex that activates factors IX and X via proteolysis 1. TF initiates cell-surface assembly of the coagulation cascade and plays critical roles in hemostasis and inflammatory responses. Beyond hemostasis, F3 has emerged as a disease-relevant gene in multiple contexts. In glioblastoma, F3 expression identifies quiescent cancer stem cells that evade chemotherapy, drive tumor initiation and recurrence, and express stem cell-associated genes 2. Pan-cancer analysis identified F3 as a venous thromboembolism-related gene with high prognostic value in glioblastoma and lower-grade gliomas, correlating with tumor stemness and predicting patient outcomes with AUC values of 0.78-0.9 3. In infectious disease, F3 upregulation links inflammation, thrombosis, and cellular senescence in COVID-19, with severe patients showing 5.2-fold increased F3 transcript expression in peripheral blood mononuclear cells 45. Inflammasome activation in sepsis triggers F3 release from macrophages and monocytes, connecting innate immunity to coagulation 6. Genetic variation in F3, such as rs2022030, associates with increased F3 expression and prothrombotic markers like D-dimer 1, establishing F3's role as both a hemostatic regulator and therapeutic target in cancer and thrombotic disease.