Considering these, we proposed that excessive glutamate release induced by pancreatitis pain may trigger calcium influx into post-synaptic membrane and subsequent intracellular signaling pathways to phosphorylate GluA1-containing AMPA receptor and NR2B-containing NMDA receptor, which promotes membrane trafficking and long-term potentiation of insular excitatory transmission. This evidence concerns the gene GRIA1 and pancreatitis.