To see whether it extends to other mouse models of neuromuscular disease, we analyzed L1-L5 DRG from SOD1G93A mice, an established model of SOD1-associated amyotrophic lateral sclerosis (ALS), which displays a plethora of defects and dysfunctional pathways in peripheral, albeit mainly motor, nerves (Kim et al., 2015; Nardo et al., 2016). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.