Increasing evidence indicates the presence of ferroptosis markers in FRDA, including increased plasmatic malondialdehyde documenting lipid peroxidation, low levels of glutathione and downregulation of GPX4 implicating lower antioxidant status, upregulation of nuclear receptor coactivator 4 (NCOA4) indicating ferritinophagy, and downregulation of NRF2, which is a natural inhibitor of ferroptosis [262]. The gene discussed is NCOA4; the disease is Friedreich ataxia.