Moreover, overexpression of the wild type forms of SOD1 [26], TDP-43 [78, 91, 92] or FUS [55] generally leads to similar, if not exacerbated, symptoms as compared to expression of the ALS-linked mutations, casting doubts on their relevance as faithful animal models of the disease. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.