Whatever the mechanism is, the hypothesis that TRAP1 S-nitrosylation plays any role in neuronal injury distinctive of PD and—at least in principle—in other neurodegenerative diseases is realistic and claims for further investigations, e.g., to identify TRAP1 clients downstream of PINK1 and understand their regulation following PINK1 and TRAP1 S-nitrosylation. This evidence concerns the gene TRAP1 and Parkinson disease.