Thus, it is conceivable that in SOD1 mutant-caused ALS, the overall decline of autophagic flux may be induced by the association of SOD1 mutants with p62/SQSTM1, although the association of the two can promote autophagy to remove misfolded SOD1 mutants to some extent in the early disease stages. This evidence concerns the gene SQSTM1 and amyotrophic lateral sclerosis.