1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced c-Abl activation leads to the Parkin inactivation, which in turn causes the accumulation of AIMP2 and neuronal death.364 Furthermore, c-Abl was activated and Parkin was phosphorylated at Tyr143 in postmortem human brain tissue from PD patients.364 Therefore, c-Abl may serve as a pathogenic kinase in PD by inhibiting the Parkin activity. Here, PRKN is linked to Parkinson disease.