This may be due to stimulation of VEGF-dependent vascular proliferation in patients with reduced VWF activity that initiates angiogenesis and encourages the development of arteriovenous malformations.9 Additionally, platelets undergo metalloproteolytic shedding of their surface receptors reducing their ability to be activated and to bind to VWF, collagen and fibrinogen.10 Thrombocytopenia and hyperfibrinolysis have also been implicated in the bleeding diathesis observed during MCS.11 This evidence concerns the gene VWF and Thrombocytopenia.