Activated platelets may also form a physical shield around tumor cells, protecting them from natural killer cell-mediated clearance and promoting distant metastasis (15, 16).This TF- and platelet-driven hypercoagulable state not only reflects enhanced tumor aggressiveness but also provides a mechanistic rationale for the prognostic significance of coagulation markers in SRRCC and highlights the potential role of anticoagulant strategies as adjunctive therapeutic approaches. The gene discussed is TF; the disease is neoplasm.