The number of children and young adolescents diagnosed with cancer is increasing, leading to a need for new therapeutic strategies with diminished neurodegenerative side- effects. This report presents preliminary observations on glioma-initiating cells (GICs) in the way to develop a strategy that induces cell-cycle arrest or quiescence in neural stem cells (NSCs). To test how changes in membrane potential due to pharmacological treatments have effects on localization and levels of REV-ERBα protein, proneural (PN) and mesenchymal (MES) cells were treated with varying concentrations of REV-ERBα agonist SR9009 drug and T-type calcium channel blocker mibefradil. Treatments showed that both drugs do not relocalize REV-ERBα to the nucleus. However, SR9009 decreases the levels of REV-ERBα protein, whereas mibefradil does not have a similar effect.  Our preliminary data on mouse NSCs showed they engage with REV-ERBα protein while going into contact inhibition. Therefore, we investigated whether high confluency put PN and MES GICs into quiescence and the role of the main molecular clock protein REV-ERBα in this process. Cells were grown up to certain confluency, and following qPCR gene expression analysis revealed PN cells go into contact inhibition whereas MES cells continue proliferating even after they are grown to confluency. Moreover, REV-ERBα protein does not have any role in both outcomes.