AKT1 and neoplasm: Molecularly, AEG-1 promotes tumor cell proliferation by suppressing forkhead box protein O1, induces serum-independent cell growth, suppresses apoptosis through activation of PI3K-Akt signaling[16-20], and increases anchorage-independent growth of non-tumorigenic astrocytes through activation of PI3K-Akt and nuclear factor-kappa B (NF-κB) pathway[17,21].