AKT1 and glioblastoma: It has been postulated that the characteristic of GBM’s intense resistance to cell death is associated with genetic alterations in regulatory molecules involved in mitogenic signaling, especially those involving the signaling pathway of phosphoinositide 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/protein kinase B (Akt) induced by hepatocyte growth factor/hepatocyte growth factor receptor (MET), the death receptor systems of the TNFR1 and TNF-related apoptosis-inducing ligand, and the anti-apoptotic BCL-2 family.