Venous thromboembolism (VTE), comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), is a multifactorial disease, involving complex interactions between individuals (including their hemostatic system and genetic predispositions) and their environmental exposures. Active malignancy is a well recognized risk factor for VTE and accounts for almost 20% of incident VTE events occurring in the community , with chemotherapy independently adding to that risk [2, 3]. As compared with the general population, the risk of VTE is increased fourfold in patients with cancer and this risk is further elevated to more than sixfold when these patients are receiving chemotherapy . Moreover, there is a twofold increase in recurrent VTE in patients with malignancy and a fourfold increase in this risk for those receiving chemotherapy . In addition, the risk of VTE varies by cancer type and stage [3-6]. The type of chemotherapy administered, hormonal treatments, immunomodulating and anti-angiogenesis agents (e.g., thalidomide, lenalidomide, bevacizumab), and supportive therapy with hematopoietic growth factors like recombinant human erythropoietins have been implicated in alterations in hemostasis and with increased VTE risk.