Phosphorylation of 4E-BP1 by mammalian target of rapamycin (mTOR), AKT, and extracellular signal–regulated kinase (ERK) prevents 4E-BP1 binding to the eIF-complex, leading to an aberrantly upregulated translational efficiency, which is an important characteristic of tumor growth, metastatic progression, and cancer stem cell enrichment [7,8]. This evidence concerns the gene AKT1 and cancer.