SOD1 and amyotrophic lateral sclerosis: This is consistent with other ALS models, as overexpression of ALS proteins induces rapid severe phenotypes in transgenic mice (Gurney et al, 1994; Mitchell et al, 2013), whilst mutations in endogenous Sod1 and Fus show slower milder neuromuscular phenotypes (Joyce et al, 2014; Devoy et al, 2017; Scekic‐Zahirovic et al, 2017).