These data suggest that under certain conditions, including genetic factors and environmental factors, SOD1WT may also serve as the cause of ALS pathogenesis and that inhibition of the SOD1-Derlin-1 interaction may be a potential target for ALS therapy development not only for SOD1mut-caused FALS but also for a subset of SOD1 mutation-negative FALS and SALS, in which conformationally disordered SOD1WT is proposed to be involved. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.