Repurposing or developing novel pharmacological therapies that are capable of addressing the many downstream consequences of dystrophin deficiency, such as FAEs and novel Nrf2 activators, respectively, may be a viable option to improve patient quality of life without severe adverse events like those observed with corticosteroid use. The gene discussed is NFE2L2; the disease is neuromuscular disease caused by qualitative or quantitative defects of dystrophin.