On the molecular level, GBM is characterized by coactivation of receptor tyrosine kinases (Huang et al., 2007; Stommel et al., 2007), activation of PI3K-AKT signaling (Li et al., 1997a; Stambolic et al., 1998), and loss of p53 and RB tumor suppressor pathway function (Furnari et al., 2007). This evidence concerns the gene RB1 and glioblastoma.