As examples, the involvement of the GluA2-containing AMPARs was demonstrated in putative mechanisms of Alzheimer’s disease [49,50], blocking the interactions of GluA2 subunits with certain proteins inhibited mechanisms of neuropathic pain [51], and GluA2 subunit flip and flop isoforms are decreased in schizophrenia [52]. The gene discussed is GRIA2; the disease is early-onset autosomal dominant Alzheimer disease.