Coagulation disturbance may be increased by activation of oncogenes (RAS, MET, EGFR) and inhibition of tumor-suppressor genes (p53, PTEN).[32] Mutations of these genes lead to the production of procoagulant agents and especially tissue factor, with activation of the extrinsic coagulation pathway, and plasminogen-activator inhibitor I.[32,33] Platelet aggregation is a result of the production of cyclooxygenase 2 and then thromboxane A2. Here, F3 is linked to neoplasm.