Immunofluorescence assays confirmed increased nuclear localization of the AP1 complex member JUN as well as β-catenin in mutant SOD1 MNs compared with the isogenic control MNs (Figures 4C and S3A), confirming activation of the AP1 and WNT pathways in ALS MNs. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.