It was also recently shown that in the presence of SOD1–ALS mutations that are able to preserve the ability of the enzyme to bind zinc or Cu, the administration of Cu(II)-diacetyl-bis(N4-methyl-thiosemicarbazone (CuATSM) can be connected with delivery and binding of Cu to SOD1, which can cause proper SOD1 maturation, increased SOD1 activity, and reduced SOD1 aggregation, as well as increased cell viability [192]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.