The impairment of ER‐mitochondria Ca2+ signaling observed in AβO‐treated cells might be explained by upregulation of mRNA levels of proteins involved in Ca2+ signaling at MAM, namely InsP3R, Sigma1R, GRP75, and VDAC1, InsP3R1‐VDAC1 direct interaction and associated augmented ER‐mitochondria coupling, in accordance with previous studies performed in AD cell and animal models before amyloid plaque formation and postmortem AD brains (Chu et al., 2021; Hedskog et al., 2013). This evidence concerns the gene SIGMAR1 and Alzheimer disease.