F2R (coagulation factor II thrombin receptor) is a G protein-coupled receptor that functions as a high-affinity thrombin receptor, mediating calcium signaling through phospholipase C activation and inositol 1,4,5-trisphosphate production 12. Beyond hemostasis, F2R regulates diverse physiological processes including platelet activation, vascular development 3, and inflammatory responses through upregulation of pro-inflammatory cytokines like IL-6 and MCP-1 45. F2R is increasingly recognized as oncogenic across multiple cancer types. In anaplastic thyroid cancer, POLR1F promotes F2R transcription via H3K4 methylation, activating p38 MAPK signaling to enhance proliferation and stemness 6. F2R expression is elevated in gastric adenocarcinoma and correlates with poor prognosis and advanced tumor stage 7. Similarly, high F2R expression in ovarian cancer associates with reduced progression-free survival, chemotherapy resistance, and increased metastatic potential; F2R suppression reduces cell motility and invasion 8. In gliomas, F2R missense variants (R214H, C378G) predict structural destabilization and altered cancer progression 9. Clinically, F2R IVSn-14 A/T polymorphisms influence clopidogrel response in stroke patients, with T-allele carriers showing reduced recurrent stroke risk 10. F2R also mediates fibroblast-endothelial interactions in tissue remodeling and contributes to psoriatic inflammation through the PRSS3-F2R pathway 1112.