The recent discovery of misfolded wild‐type SOD1 deposition in the vulnerable SNc of Parkinson's disease patients[13, 166a] indicates that modulation of SOD1 biochemistry may partially underlie the putative therapeutic efficacy of CuII(atsm) in Parkinson's disease animal models, similar to that observed in mutant SOD1 transgenic mice. Here, SOD1 is linked to Parkinson disease.