Frataxin activates persulfide transfer, which is essential for the assembly of iron–sulfur clusters (Fe–S) in the mitochondria and the activity of the mitochondrial respiratory chain complex and other mitochondrial enzymes.419,420 Mitochondrial iron accumulation, energy imbalance, increased ROS, and lipid peroxidation are all related to the pathogenesis of this disease, suggesting that ferroptosis may be closely related to Friedreich’s Ataxia.421–424. This evidence concerns the gene FXN and Friedreich ataxia.