Another study showed that CACNA2D3 could increase intracellular Ca2+ levels and promote apoptosis in nasopharyngeal cancer and glioma, causing changes in the network of tumor-suppressive properties and inducing upregulation of Nemo-like kinase (NLK) through the non-canonical Wnt/Ca2+ signaling pathway (14, 18). Here, CACNA2D3 is linked to neoplasm.