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. This evidence concerns the gene NFKB1 and glioblastoma.