It has been demonstrated that the expression of modulators of calcium flux on glioblastoma cells, such as FPRL-1 (formyl peptide receptor-like 1), GluRs (Glutamyl-tRNA synthetase) and P2 × 7R (an ATP-gated nonselective cation channel) along with voltage-gated calcium channel, activate the signaling pathways of MAP Kinases, as well as AKT and PI3K, hence triggering survival, growth and mobility of GMB cells [4,40,41]. Here, AKT1 is linked to glioblastoma.