FTMT and Friedreich ataxia: The presence of “free” chelatable iron in mitochondria of MEOAL patient cells (Fig. 7C) suggests that the storage capacity of FtMt is overcome and this could explain both the increased mitochondrial basal production of ROS that we observed by MitoSoxRed staining (Fig. 8A) and the higher sensitivity to pro-oxidant conditions (Fig. 8B), as previously found in other neurodegenerative diseases associated with dysfunctional FeS clusters assembly process, such as Friedreich ataxia [57].