Various factors contribute to the pathogenesis of ALS including mutations in the SOD1 gene, mutations in the ALS2 (Alsin)[1,2], FUS (RNA-binding protein FUS)[3], TARDBP (TAR DNA-binding protein 43)[4,5], ATXN2 (Ataxin-2)[6] and ANG (Angiogenin)[7] genes, and the recently-discovered intronic hexanucleotide expansions in C9ORF72[8,9]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.