Numerous morphological and functional alterations of mitochondria have been reported in the pathogenesis of SNCA and parkin (PARK2 or PARK7) mutant hiPSC models of PD (33–36), in models of AD (37, 38), and in TDP-43, FUS, and superoxide dismutase 1 (SOD1) mutant models of ALS (39). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.