Conversely, genetic reduction of IP3R1 normalizes disturbed Ca2+ signaling in PS1-M146V KI mice and most importantly alleviates AD pathogenesis (i.e., rescues aberrant hippocampal long-term potentiation (LTP), attenuates Aβ accumulation and tau hyperphosphorylation and memory deficits) in both PS1-M146V KI and 3xTg-AD mice [72]. The gene discussed is ITPR1; the disease is Alzheimer disease.