Together, our data suggest that schizophrenia-related missense mutations that inhibit the ability of βSAP97’s PDZ2 domain to interact with GluA1 (Fig. 5c) should produce a potentially pathological release of GluA1-containing AMPARs into the glutamatergic synapses of DG granule neurons. The gene discussed is GRIA1; the disease is schizophrenia.