Anticancer drugs are capable of inducing thrombogenic effects through multiple different mechanisms: (1) release of procoagulants and proinflammatory cytokines from damaged neoplasm cells; (2) direct drug toxicity on the vascular endothelium; (3) direct induction of monocyte or tumour-cell expression of TF; (4) a decrease in physiological anticoagulants; and (5) platelet activation and aggregation. The gene discussed is TF; the disease is neoplasm.