A landmark discovery in ALS research was the finding that mutations in the gene encoding the enzyme superoxide dismutase SOD1 are responsible for 20% of inherited ALS cases, where normal SOD1 is a crucial intracellular antioxidant, facilitating the clearance of the potentially toxic superoxide radicals and protecting cells from reactive oxygen species (ROS)-mediated damage, such as the formation of toxic oligomers and protein aggregates from misfolded proteins [76]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.