In experimental DKD, the increase in reactive oxygen species (ROS) (article number 5) and NAD(P)H oxidase levels (article number 22, 63, 67, and 91), activation of PKC (article number 24 and 81), decrease in eNOS (article number 55, 85, and 100) and mitochondrial dysfunction (article number 70, 72, and 89) promote OS injury, while Nrf2 (article number 45, 73, and 88) protects the kidney from OS in DKD as an antioxidant factor. This evidence concerns the gene PRRT2 and diabetic kidney disease.