Interestingly, in levodopa-induced dyskinesia, Src S-nitrosylation was caused by a neuronal nitric oxide synthase (nNOS)/NO signal activated by Ca2+ influx via GluN2B-containing NMDAR, which subsequently facilitated Src autophosphorylation (at Tyr416) and further phosphorylated GluN2B, demonstrating a positive feed-forward effect leading to GluN2B Tyr phosphorylation [35]. This evidence concerns the gene NOS1 and drug-induced dyskinesia.