AKT1 and glioblastoma: These observations support a critical role for intragenic EGFR gene deletions and EGFR gene amplification since cross-talk between the intragenic EGFRvIII deleted variant and EGFR amplification, leads to constitutive activation of the PI3K-AKT signaling pathway and, which might ultimately contribute to explain malignant transformation in GBM [31], as previously suggested by others [22,30].