PINK1-Parkin double knockout results in the accretion of damaged mitochondria, which lowers mitochondria function and causes degeneration of ALS neuromuscular junctions.214 Conversely, Palomo et al. reported that in the SOD1-G93A mouse model, ablation of the Parkin gene reduces mitochondria depletion and delays ALS progression.178 However, to date, there has been no plausible explanation for these discrepancies. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.