Possible mechanisms to explain the prothrombotic nature of BD in literature include: progressive decline in endothelial progenitor cells, direct endothelial injury, aberrant fibrinogenolysis and platelet activity, abnormal levels and expression of thrombomodulin, adrenomodulin and vascular endothelial growth factor (VEGF), E-selectin activation and variable nitric oxide levels [5,36]. The gene discussed is VEGFA; the disease is Behcet disease.