Overall, the presence of anti-GluA3 Abs in FTD patients corroborates other evidence claiming a possible role of AMPARs in FTD pathogenesis: The hyperexcitability of AMPARs contributed to neurodegeneration [72]; social deficits were accompanied by a change in AMPAR composition in an animal model of FTD [72]; frontal cortex and human-induced pluripotent stem cells (hiPSCs) of behavioral-variant FTD patients showed changes in AMPARs [73]; and the physiological release of Tau protein was mediated by AMPARs [74]. The gene discussed is MAPT; the disease is frontotemporal dementia.