Communication with Ca++ signaling occurs via gap junctions in glioma cells and activation of ATP‐sensitive potassium channels can upregulate Cx43 expression and increase gap junction communication, while blockage inhibits proliferation (Hitomi et al., 2015; Princen et al., 2001). Thus, we predict that disruption of cell‐to‐cell communication should reduce tumor robustness, making it more vulnerable to cytotoxic therapies. This evidence concerns the gene GJA1 and central nervous system cancer.