AKT1 and neoplasm: The reported mechanism for the tumor-suppressive role of MIIP includes reducing the stability and activity of HDAC6 [12], interacting with CDC20 to interfere with the function of APC/C acting as an ubiquitin-ligase E3 for cyclin B1 degradation [13], interaction with PP1α and negative modulating AKT signaling [14], and regulating activity and expression of NF-κB [2, 11].