All these findings suggest that some of the SOCE components, namely STIMs, RyR, and IP3R, are involved in the early dysregulation of Ca2+ homeostasis in AD and highlight the importance of further mechanistic studies to dissect the molecular pathways for the development of new drugs against early stages of AD progression associated with SOCE Ca2+ dysregulation. The gene discussed is ITPR1; the disease is Alzheimer disease.