On the other hand, impaired NO production may also have resulted from increasing endogenous NOS-inhibitor, asymmetric dimethylarginine (ADMA) in patients with end-stage renal disease, which is well documented in previous studies.[17, 23] However, one of the limitations in this study was the inability to separate the various isoforms of NOS (endothelial, neuronal, and inducible). The gene discussed is NOS1; the disease is chronic kidney disease.