The implication of NO in PD pathogenesis is supported by the observations that iNOS expression is upregulated in activated microglia [11], [45], the immunoreactivity of nitrated α-synuclein is prominently positive in the Lewy bodies [46], [47], and several enzymes including parkin, peroxiredoxin-2, and protein-disulphide isomerase lose their function by S-nitrosylation in PD brains [48]–[50]. The gene discussed is NOS2; the disease is Parkinson disease.