Under oxidative stress conditions, Keap1 is oxidized at reactive cysteine residues, resulting in inactivation of Keap1 and stabilization of Nrf2, which then translocates into the nucleus and subsequently binds to antioxidant response elements to promote the expression of downstream cytoprotective proteins that act as scavengers for diabetes-induced free radicals [103–105]. The gene discussed is KEAP1; the disease is diabetes mellitus.