Although to different extent, all of these treatments were able to prevent or revert SOD1 aggregation in neuronal cells, ameliorating mutant G93A-SOD1 protein solubility, preserving mitochondrial function and preventing apoptosis, thus suggesting that modulation of the redox state of cysteine residues in specific compartments could be a significant therapeutic strategy for ALS. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.