Such genetical insights and the observation that the clinical courses of sALS and fALS were similar in several aspects prompted the production of Tg mouse models bearing SOD1 mutations different from hSOD1(G93A) (and of other fALS-related genes) for the study of ALS pathomechanisms [67,68,69]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.