Moreover, non-native formations of wild-type SOD1 have been observed in small granular SOD1-immunoreactive inclusions in sALS patient motor neurons and in patients harboring the C9ORF72 repeat expansion and pathogenic variants in other ALS-associated genes [77,78], suggesting that both mutant and wild-type SOD1 forms harbor the potential to misfold and cause ALS. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.