As studies have indicated a substantial contribution of CNVs to the etiology of neuropsychiatric disorders (NPDs),4, 5, 6, 7 the identification of CNVs in PRKN among patients with schizophrenia (SCZ) and autism spectrum disorder (ASD) has brought the possible involvement of PRKN in NPDs to light8, 9 This is further supported by neurobiological evidence that knockdown of Parkin causes reduced surface levels of AMPA and NMDA receptors and alters glutamatergic synaptic transmission, which is a common feature of synaptopathy in SCZ and ASD.10, 11, 12. This evidence concerns the gene PRKN and schizophrenia.