AKT1 and glioblastoma: GBM resistance to conventional proapoptotic chemotherapy and radiotherapy results from changes at the genomic, transcriptional, and posttranscriptional level in key molecules involved in mitogenic signaling, mostly in the PI3K/PTEN/Akt axis, in tyrosine-kinases receptors (RTKs) and their ligands, and in regulatory molecules and effectors of the apoptotic cell death pathway [148, 150].