Our results demonstrate that one of the most important downstream targets for the absence of STIM1 in differentiated neuroblastoma cells is the upregulation of Ca2+ influx through Cav1.2, which fully explains the Ca2+ dysregulation observed in hippocampal neurons from model animals as well as the protective effect of VOCCs inhibition in AD patients. The gene discussed is STIM1; the disease is Alzheimer disease.