AKT1 and cancer: From the comparable stability of MDM2 protein in BPH-1 cells and CAFTD clones and the increased activation of the Akt signaling pathway in CAFTD clones (Supplementary Figure S2D, [24]), we surmised that Akt-phosphorylation-mediated MDM2 stabilization via decreased ubiquitination [34] is unlikely to contribute to the mechanism of MDM2 regulation in our cancer models.