These mainly included cancer cells expressing proteins that could alter the number of platelets and leukocytes in circulation (such as IL6, MUC1, MUC16, and MUC5AC) [46] and the expression of procoagulant proteins such as TF and PDPN, which could directly activate the coagulation cascade and upregulation of antifibrinolytic/anticoagulation proteins (PAI1 and HPSE) [47–50]. The gene discussed is IL6; the disease is cancer.