Building on the established metabolic phenotypes of mesDA neuronal subpopulations—particularly the high metabolic demand of SNpc neurons and their dorsal striatum projections (5, 9, 10), which may contribute to their selective vulnerability in PD—and our previous work demonstrating DJ-1 as a key regulator of neuronal metabolic efficiency, we postulated that metabolic efficiency, through this mechanism and DJ-1-β-sub association, is differentially regulated in SNpc and VTA neurons, with the association levels potentially altered in PD. This evidence concerns the gene PPIB and Parkinson disease.