Cancer itself is a well-known risk factor for thrombosis development through various simultaneous mechanisms involving venous stasis (immobilization and compression), endothelial damage (cancer-associated and from surgery, chemotherapy, and central venous catheters), and blood hypercoagulation (from expression of tissue factors and cancer-associated pro-coagulants, and associated with therapy using hormones, asparaginase, corticosteroids, etc.)[7, 8]. This evidence concerns the gene ASPG and cancer.