Since 1993 variants in more than 40 genes (SOD1, NEFH, SETX, ALS2, DCTN1, HFE, VAPB, ANG, CHMP2B, TARDBP, UNC13A, ELP3, FUS, ATXN2, OPTN, SPG11, VCP, C9ORF72, SQSTM1, UBQLN2, ATXN1, EPHA4, PFN1, HNRNPA1,CHCHD10, MATR3, TUBA4A, TBK1, CCNF, NEK1, C21ORF2, TIA1, ANXA11, KIF5A, GLT8D1, ARPP21, DNAJC7, WDR7, CAV1, SPTLC1 and so on) have been shown to cause ALS, increase ALS risk or be linked to a difference in the clinical phenotype of Amyotrophic Lateral Sclerosis (n.d.). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.