AKT1 and cancer: Cancer cells of patients diagnosed with GCB-DLBCL are frequently addicted to PI3K/Akt signaling, and degradation of Myc can be inhibited as a consequence of Akt-induced inactivation of GSK-3β, whereas sequestering of Bcl-2 can be disrupted by Akt-induced phosphorylation of the proapoptotic protein Bad [49, 58, 59].