Considering their substantial morbidity and mortality rates, tumors of the brain and central nervous system (CNS) are among the most fatal cancers. [1] Among them, gliomas are the most common malignant forms of cancer. Regarding the growth mechanism of gliomas, the surrounding microenvironment and local network activity among tumor cells are key areas of interest. The oscillations of brain activity are also directly related to tumor growth and can be induced by external stimuli. Out of the relevant signals and biomarkers, calcium ion (Ca 2+ ) channels and signaling dynamics show the greatest correlation with oscillatory brain activity. The activity of intracellular Ca 2+ oscillations can be used to characterize promoters like ASCL-1 or neurogenin-2, which are related to luciferase reporter genes. [2] Characterizing these promoters helps to link the micro genes information and macro detectable information.Recent research has focused on glioma cell network communication via Ca 2+ transients and KCa3.1, a type of Ca 2+ -activated potassium ion (K + ) channel. [3] These network communications can protect glioma cells after surgery, leading to local tumor recurrence. Glioma cells are closely connected to multicellular networks, and Ca 2+ transients are transferred between individual cells through interconnecting tumor microtubes. This results in rhythmic Ca 2+ fluctuations that periodically activate signaling pathways like MAPK and NF-κB, increasing the proliferation of tumor cells and promoting tumor growth. Glioma cells that display such periodic Ca 2+ activity are known as periodic cells. Inhibiting cellular entry and chelation of Ca 2+ or inhibiting tumor cell connectivity via gap junctions can also strongly reduce the proliferation of glioma cells. As a result, the rhythmic Ca 2+ activity in glioma cell networks is a tumor cell-autonomous functional state, which is not affected by the external environment.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.