Thus, considering the importance of L-VGCC in the central nervous system and Ca2+ being such an important regulator of synaptic plasticity, we could suppose that a disruption in CACNA1D, CACNA2D3, and CACNA2D3 caused by CNVs may lead to a dysregulation in Ca2+ homeostasis and contribute to the pathogenesis of AD. The gene discussed is CACNA2D3; the disease is Alzheimer disease.