Multiple factors and mechanisms have been suggested for the eNOS upregulation or activation (e.g., high glucose, VEGF, IGF-1, and shear stress), for the eNOS dysfunction, inactivation, and downregulation (e.g., ROS, angiotensin II, AMDA, PKC, AGE, and TNFα), and for reduction of NO bioavailability (e.g., excessive superoxide production) in DN [2, 31]. The gene discussed is AGT; the disease is liver dysplastic nodule.