Furthermore, the aortic tension experiments showed that xyloketal B significantly improves endothelium-dependent, NO-mediated vasorelaxation to acetylcholine (Ach); whereas this treatment effect was eliminated in the presence of eNOS blocker N-nitro-l-arginine methyl ester (l-NAME), suggesting that xyloketal B may improve endothelial dysfunction through enhancing NO bioavailability [16]. The gene discussed is NOS3; the disease is endothelial dysfunction.