Neuronal dysfunction in AD has been described to be mediated by AβO‐induced intracellular Ca2+ dyshomeostasis through mGluR5 overactivation, leading to elevated ER‐Ca2+ accumulation (Zhang et al., 2015), and through GluN2B‐composed NMDAR (Ferreira et al., 2012, 2015), which leads to mitochondrial Ca2+ overload as a consequence of ER‐Ca2+ release through InsP3R (Ferreira et al., 2015). The gene discussed is GRM5; the disease is Alzheimer disease.