The disruption of signal transduction in GBM occurs through over-expression or a gain-of-function mutation of tyrosine-kinase receptors6, 7, thus leading, among other events, to constitutive activation of Ras/extracellular signal-regulated kinase (ERK), AKT/mammalian target of rapamycin (mTOR). This evidence concerns the gene AKT1 and glioblastoma.