These findings are interesting because mitochondrial dysfunction and the formation of reactive oxygen species are thought to occur in SOD1 mutation carriers as well as patients with C9ORF72 mutations, mutant TDP43, and FUS during ALS pathogenesis (Lopez‐Gonzalez et al., 2016; Onesto et al., 2016). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.