The biggest bottlenecks that prevent the translation of these biological findings into PD therapies are (i) the lack of detailed knowledge on the structure of the normal and mutated versions of the proteins, (ii) the reliance on harsh stressors to activate this pathway, and (iii) limited understanding of the exact downstream molecular players involved in PINK1-Parkin-mediated neuroprotection. This evidence concerns the gene PRKN and Parkinson disease.