In mice, SOD1 loss-of-function does not result in neurodegeneration, whereas ubiquitous overexpression of mutant SOD1 leads to ALS-like symptoms, including those mutant SOD1 genes with a normal dismutase function (Bruijn et al. 1997; Gurney et al. 1994; Wong et al. 1995). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.