As expected, upon mitochondrial membrane depolarization, we found the levels of OMM proteins and Parkin substrates significantly increased in the neurons of the homozygous PRKN-PD line compared to the control neurons, consistent with impaired Parkin-dependent degradation, as observed previously for both PRKN and PINK1 knockout animals and mutant human fibroblasts45,46. This evidence concerns the gene PINK1 and Parkinson disease.