KEAP1 and Friedreich ataxia: This leads to a conformational change in the Keap1‐Nrf2 complex, whereby Nrf2 escapes Keap1‐induced degradation, translocates to the nucleus, and activates the expression of antioxidant and cytoprotective genes.[10, 11, 12] Covalent Nrf2 activators‒such as the marketed drugs dimethyl fumarate (DMF) and omaveloxolone for multiple sclerosis and Friedreich's ataxia‒directly react with the Keap1 cysteines.