Moreover, given the recent link between PARK2 copy number variation and neurodevelopmental disorders, our findings further underscore the importance of elucidating Parkin’s molecular mechanisms of action at glutamatergic synapses, both to facilitate the development of better treatments for motor and non-motor symptoms of PARK2-linked PD, and to shed light on its emerging role in the etiology of neuropsychiatric disease. The gene discussed is PRKN; the disease is neurodevelopmental disorder.