In the past decades, a body of literature has demonstrated that nitric oxide (NO) produced by endothelial cells through the endothelial nitric oxide synthase (eNOS) plays a major role in regulation of vascular homeostasis including vascular tone, coagulation and platelet aggregation, and inflammation [8] and that eNOS deficiency advances a variety of renal diseases in mice, including diabetic nephropathy and remnant kidney injury [9, 10], indicating a critical role of eNOS in the progression of renal disease. This evidence concerns the gene NOS3 and kidney disorder.