MTOR and glioblastoma: Moreover, this mTORC2-NF-κB pathway makes cells and tumors of GBM resistant to chemotherapy in a manner independent of V-akt murine thymoma viral oncogene homolog (AKT).89 Furthermore, the EGFRvIII and wild-type EGFR strongly activate the RAS/MEK/ERK signaling, the PI3K/AKT/mTOR signaling, the Notch signaling, and the signal transducer and activator of transcription (STAT) 3/5 signaling.90–92 These signalings functions in the regulation of cell activities.91 This is one of the grounds for targeting these signaling pathways to treat GBM, which will be elaborated on later.