The limitations of the study are three-fold: (1) Our analyses on the glioma-neuron interaction was mostly limited to in vitro cell-based assays, and exploitation of in vivo and ex vivo brain tumor models, supported by electrophysiological methods [40, 41], would be essential to further unravel how hypomethylated glioma cells could interact with neuron in the brain; (2) Assessment of the other lines of inquiry, including mTOR-FAK mechanotransduction signaling axis, was rarely performed in addition to the one on glutamate network reprogramming. The gene discussed is PTK2; the disease is glioma.