No overlap was observed between p62 and pTDP-43 pathologies in SOD1-fALS cases, and therefore motor neurons exhibiting p62 pathology in the absence of mutant disSOD1 (24% of total surveyed population) may reflect efforts by p62 to promote the clearance of additional ALS-linked proteinopathies not examined in this study, including FUS [27]. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.