Furthermore, CuII(atsm) treatment reportedly mitigates nitrosative stress[205] and neuroinflammation[232] in vivo, and promotes neurite elongation in vitro,[233] suggesting other neuroprotective actions of CuII(atsm) in ALS that are largely, if not completely, independent of SOD1. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.