AKT1 and neoplasm: AKT activated by phosphorylation, which includes the binding of PI3K-phosphorylated phosphoinositides (PI) called PIP3 AKT pleckstrin homology domain and subsequent translocation to the plasma membrane and phosphorylation at two phosphorylation sites Thr308 and Ser473 by PDK1 and PDK2, respectively, resulting in its activation in tumor cells, so it was found that direct degradation of AKT deregulated AKT activity and promoted an apoptotic process [9,10,11].