MTOR and glioblastoma: Further evidence suggests that D-2HG supports a metabolic change (hypermetabolic phenotype) in GBM surrounding neurons, characterized by lactic dehydrogenase-A increase, defects in the tricarboxylic acid cycle [56,57], as well as upregulation of mTOR (mechanistic target of rapamycin) activity [56,58], already known as pro-epileptogenic stimuli.