However, in ECV304 cells, a model of endothelial dysfunction associated with type 2 diabetes, HTyr (10 μM, 48 h) significantly increased endothelin-1 (ET-1) expression, enhanced eNOS phosphorylation, and increased nitric oxide production, thereby partially counteracting endothelial dysfunction induced by high glucose and free fatty acids [168]. The gene discussed is EDN1; the disease is type 2 diabetes mellitus.