AKT1 and neoplasm: Upregulation of caspase-3, caspase-9, p16, p21, p53, TRAIL, pro-apoptotic BAX, ATG5, ATG7, BECLIN1 and cellular H2O2 levels [148, 167–170, 173, 180, 182]; activation of Smac/DIABLO [173]; and downregulation of survivin, XIAP, cyclin D1, Cdk4, Cdk6, cyclin A2, cyclin E1, AKT/pAKT, Bcl-2, β-catenin, c-Myc, pro-caspase-7, PCNA, Bcl-xL and MMPs have been demonstrated to be involved in the MSC-dependent tumor cell apoptosis seen with MSC-CM, MSC cell lysate (CL) and with direct cell–cell interaction [167, 168, 170–176, 178, 180].