VEGFA and neoplasm: The development of DVT may result from the anti-VEGF effect of bevacizumab whereby VEGF inhibition enhances coagulation by exposing subendothelial procoagulant phospholipids, reduces production of nitric oxide and prostacyclin by endothelial cells, increases hematocrit and blood viscosity via overproduction of erythropoietin, increases expression of proinflammatory cytokines, and possibly increases the release of procoagulant from the tumor into the blood stream due to an enhanced cytotoxic effect [8–11].