GRIA1 and schizophrenia: Altogether, our data demonstrate that both reduced βSAP97 expression and schizophrenia-related missense mutations in βSAP97’s PDZ2 domain compromise βSAP97’s interaction with GluA1-containing AMPARs and, as a result, cause rearrangements of AMPARs present on the dendritic surface of DG granule neurons that lead to increased AMPAR expression in the PSDs of existing functional glutamatergic synapses.