Frataxin-knockout mouse myoblasts, heart, and skin fibroblasts all showed characteristics of ferroptosis, and Nrf2 was downregulated in Friedreich’s Ataxia patients and frataxin-knockout mice, while Nrf2 activators EPI-743 or sulforaphane regulated redox imbalances and rescued ferroptosis in frataxin knockout cells.436. This evidence concerns the gene NFE2L2 and Friedreich ataxia.