EGFR and glioblastoma: Conversely, the expression of EGFRvIII, an active EGFR mutant, or the activation of mTOR complex 1 (mTORC1) through silencing the expression of its inhibitor tuberous sclerosis 2 (TSC2) exacerbates ATP depletion and increases the sensitivity of GBM cells to hypoxia-induced cell death [9, 10].