Endothelin-1, an inflammatory mediator, can stimulate macrophages and monocytes to release proinflammatory cytokines.[7] Endothelial dysfunction (ED) is a constant feature of BD.[8] Overexpression of proinflammatory cytokines, adhesion molecules, free oxygen radicals, and high homocysteine levels have been suggested to be responsible for the activation of endothelial cells, irrespective of overt vascular manifestations.[9]. This evidence concerns the gene EDN1 and Behcet disease.