Diabetic nephropathy is a well-known microvascular complication of chronic hyperglycemia, and both oxidative stress and an impaired response by the Nrf2/Keap1/ARE system have been implicated in its progression via renal cell apoptosis, fibrosis, and deficiencies in cellular regeneration [11, 108, 109]. This evidence concerns the gene KEAP1 and diabetic kidney disease.