Indeed, the mutant SOD1 has been shown to exert its toxicity through misfolding and aggregation [11,12,13], and a recombinant monoclonal antibody that selectively binds to misfolded SOD1 has been shown to reduce misfolded SOD1, thus potentially delaying the onset and slowing the progression of ALS in mice [14]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.