Several studies have been performed to understand the cellular mechanisms involved in the development of VTE in cancer patients. The pathogenesis of a thrombotic state is linked to the presence of a tumor and is associated with the development of a hypercoagulant state, namely coagulopathy, which confers numerous advantages to the cancer cells. Indeed, both activation of the coagulation cascade and aggregation of blood platelets around cancer cells protect themselves from the immune response; facilitate their circulation in the bloodstream and their adhesion at potential sites of metastasis. Beside its implication in the activation of coagulation, the TF/FVIIa complex also influences pathways that activate cell-bound protease activated receptors (PARs) leading to the activation of inflammatory and angiogenic responses. Furthermore, a soluble variant of TF, known as alternatively spliced TF (asTF) stimulates angiogenesis independent of FVIIa. This leads to a model in which the presence of Tissue Factor (TF), generation of thrombin and platelets activation all directly participate to the cancer progression and dissemination. The presence of TF and the activation of platelets participate to the progression of the tumor.