Preclinical and clinical research show that tumour growth is dependent on angiogenesis. Activation of the coagulation cascade is commonly found in patients with cancer. We propose that platelets contribute to tumour-induced angiogenesis. The basis of our hypothesis is that platelets are a rich source of stimulators and inhibitors of angiogenesis and their interaction with the endothelium. Presumably, the antithrombotic state of normal endothelium is disturbed by endothelial stimuli derived from tumour cells. This hypothesis may explain the suggested clinical benefits of anticoagulants in cancer and implies that targeting of platelet interaction with tumour vasculature will inhibit angiogenesis.