AKT1 and glioblastoma: It was proposed that, in glioblastoma cells harboring EGFR amplification and the EGFRvIII mutant, wild-type EGFR promotes glioblastoma cell invasion through classical EGFR signaling pathways, while constitutively active EGFRvIII promotes angiogenesis through activation of different angiogenic pathways (Src, c-Myc, and AKT) [34].