Decreased NMDAR activity is suggested as a mechanism in the pathogenesis of psychotic illness not only by the pharmacologic and genetic evidence presented in this report, but also by (1) clinical immunology, where autoantibodies against NMDAR subunits (including the GluN2A subunit) downregulate NMDAR activity and cause a psychotic illness that clinically can be indistinguishable from schizophrenia [6] and (2) rodent models of NMDA receptor hypofunction, where restoring NMDA receptor activity rescues psychosis-like phenotypes [7]. Here, GRIN2A is linked to psychotic disorder.