Consistent with this idea, adenoviral expression of Dok-7, an inside-outside activator of MuSK, not only extends longevity of SOD1-G93A mice but also provides benefit in other mouse models of neuromuscular disease, including congenital myasthenia and Emery-Dreifuss muscular dystrophy (Miyoshi et al., 2017; Arimura et al., 2014). This evidence concerns the gene SOD1 and congenital myasthenic syndrome.