SOD1 and amyotrophic lateral sclerosis: These include mutants generated by random N-ethyl-N-nitrosourea mutagenesis of the mouse genome, for example, to produce the Sod1-D83G mouse, which has an identical mutation (aspartic acid mutated to glycine at residue 83 ‘D83G’ of superoxide dismutase 1) as found in human SOD1-ALS families (Joyce et al. 2015).