While several normal effectors of RTK and PI3K signaling, such as Ras, Akt, and mTor, are used by EGFR and PI3K in GBM and are required for gliomagenesis [1], constitutive activation of RTK and PI3K pathways may evoke changes distinct from those induced by normal developmental signaling. This evidence concerns the gene MTOR and glioblastoma.