Endothelial dysfunction and altered coagulation are typical features of BD vasculitis, and consistently with these aspects of the disease, several genes involved in vascular damage are modulated in BD specimens, including thrombospondin 1, THBS1; protein S alpha, PROS1; plasminogen activator, urokinase receptor, PLAU-UPAR; thrombomodulin, THBD; and vascular endothelial growth factor A, VEGFA. The gene discussed is PLAU; the disease is vasculitis.