We speculate this may underlie the increased interaction between p62 and mutant SOD1, compared with wild-type SOD1, in our ALS cases; namely 4- and 8-fold increases in the spatial overlap between disordered SOD1 and p62 pathologies in motor neurons of SOD1-fALS cases compared with non-SOD1-fALS and sALS cases, respectively. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.