Further analysis showed that mutations in IDH1/2-TET2 axis and mTORC1 signaling (including PTEN and EGFR mutations alone, respectively, and PTEN-EGFR mutations) display mutual exclusivity in LGG and GBM (Fig. 6e), suggesting that abrogation of PTEN function or oncogenic activation of EGFR might not confer a growth advantage to tumors carrying IDH1/2 and TET2 mutations, or that IDH1/2 and TET2 mutations might mimic PTEN loss or EGFR mutation-induced mTORC1 activation, which leads us to hypothesize that tumors with loss-of-function mutations in TET2 might be sensitive to mTORC1 suppression. Here, EGFR is linked to glioblastoma.