In contrast to molecular replacement with wild-type βSAP97 (Figs. 1d, 5j), we found that both schizophrenia-related mutant forms of βSAP97 produced dramatic increases in synaptic AMPAR-eEPSC amplitude in DG granule neurons like that seen with knockdown of βSAP97 and molecular replacement of GluA1 with GluA1-Δ7 (Fig. 5i, j). This evidence concerns the gene GRIA1 and schizophrenia.