Abnormal Ca2+ signaling is regarded as a central pathological event in AD development.[10] Multiple Ca2+ channels and signal transduction systems are altered in AD, including excessive Ca2+ release from the endoplasmic reticulum mediated by the ryanodine receptor (RyR).[11] Notably, an abnormal increase in RyR‐Ca2+ signaling leads to the defect of autophagy and overaccumulation of phosphorylated tau (pTau) protein.[12] This demonstrates that normal RyR‐Ca2+ signaling and autophagy are crucial in eliminating AD‐related pathogenic proteins. This evidence concerns the gene RYR2 and Alzheimer disease.