Haemostatic dysfunction and hypercoagulability in cancer patients is complex with a multifactorial aetiology that includes expression of procoagulant molecules such as tissue factor on the surface of malignant cells, release of fibrinolytic peptides, inhibition of endogenous anticoagulation, release of cytokines by cancer cells, and interaction with host cells including endothelial cells and blood leukocytes [28,32]. This evidence concerns the gene F3 and cancer.