The genetic component of the pathogenesis in 70% of individuals with familial ALS has been identified; mutations in chromosome 9 open reading frame 72 (C9orf72) (40%), superoxide dismutase 1 (SOD1) (20%), fused in sarcoma (FUS) (5%), and TAR DNA-binding protein 43 (TARDBP encoding TDP-43) (5%) [2]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.