In a recent study, Ha and colleagues [97] reported that mitochondrial components, including nuclear respiratory factor 1 (NRF-1), ATP synthase F1 subunit α (ATP5A), ATP synthase F1 subunit β (ATPB), and voltage dependent anion channel 1 (VDAC1), were reduced in EVs secreted by astrocytes of Fmr1 KO mice, a model of FXS. The gene discussed is FMR1; the disease is fragile X syndrome.