In this study, enhanced levels of glomerular nitrotyrosine and the upregulation of endothelial NO synthase (eNOS) by EC-NOX5 expression suggest that superoxide derived from EC-NOX5 potentially utilizes endothelial NO to form nitrotyrosine, leading to the diminished bioavailability of NO, thus causing endothelial dysfunction followed by the promotion of renal injury in diabetes. The gene discussed is NOX5; the disease is diabetes mellitus.