First, mechanistic work should integrate spatial metabolomics and mitochondrial proteomics to map ferroptosis pathways in cerebellar, spinal, and cardiac tissues from FRDA patients, with emphasis on the interaction between the iron–sulfur cluster synthesis complex (NFS1–ISCU–ISD11) and ferroptosis-related molecules (GPX4, Nrf2). The gene discussed is GPX4; the disease is Friedreich ataxia.