In the light of the proposed toxicity of SOD1 oligomers and aggregates in ALS, possible strategies to counteract aggregation such as the modulation of the GSH/GSSG ratio (Ferri et al., 2006), the overexpression of cytosolic glutaredoxin 1 (Cozzolino et al., 2008) or mitochondrial glutaredoxin 2 (Ferri et al., 2010) and treatment with cisplatin (Banci et al., 2012), that binds Cys111, i.e. the crucial residue in SOD1 aggregation, have been tested. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.