Additionally, expression of the mutant SOD1G93A gene—an ALS-associated variant of the superoxide dismutase 1 (SOD1) gene—impairs BAF60c-mediated myogenesis by upregulating HDAC4 and suppressing the Akt/p70S6K and MAPK signaling pathways, thereby disrupting the BAF60c–SWI/SNF complex and downregulating key myogenic regulators (Martini et al., 2015). Here, SOD1 is linked to amyotrophic lateral sclerosis.