It has been demonstrated that increased levels of AEA, following chronic administration of the FAAH inhibitor URB597 in a rat model of hypertension [210], significantly enhanced the expression of the CB1, thus preventing the hypertension-induced decrease of SOD, glutathione (GSH) and glutathione transferase (GT) activities and consequently lowering ROS generation and inducing hypotension. This evidence concerns the gene SOD1 and hypertensive disorder.