The significant dysregulation of neuroactive ligand-receptor interactions drives characteristic clinical manifestations in glioma: Tumor cells abnormally secrete neurotransmitters such as glutamate, which not only induce peritumoral epilepsy by activating neuron-associated receptors but also directly accelerate tumor proliferation and metabolic reprogramming through autocrine activation of the mTOR signaling axis. Here, MTOR is linked to glioma.