In terms of the regulation of intracellular Ca2+ by OM-MSCs during cerebral ischemia/reperfusion when SPCA1 was knocked down, the possible mechanisms were as follows: firstly, OM-MSCs reduced the oxidative stress level through other feasible pathways, which inhibited the Ca2+ influx from extracellular stores and the endoplasmic reticulum, eventually leading to a decline in the Ca2+ concentration of the cytoplasm. This evidence concerns the gene ATP2C1 and Cerebral ischemia.