Specifically, overexpression of mRNA or protein in some animal models and transfected cells make the models non-physiological, possibly producing phenotypes that are contrary to those observed from ALS patients with a single copy of a mutant SOD1 gene (Ludolph et al., 2010; Philips and Rothstein, 2015; Morrice et al., 2018). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.