In addition, our previous investigations have indicated that LOE is a potent inducer of NO-mediated relaxations in aortic rings and stimulator of the PI3-kinase/Akt-dependent phosphorylation of eNOS at the activator site Ser 1177 and, also, that LOE prevented the angiotensin II-induced hypertension and endothelial dysfunction in rats [27]. The gene discussed is AKT1; the disease is endothelial dysfunction.