AKT1 and acute lymphoblastic leukemia: Moreover, NOTCH1 could control mTORC1 signaling through yet another mechanism, as documented by a study in which the treatment of T-ALL cell lines with a γ-secretase inhibitor (GSI) targeting NOTCH1 resulted in the dephosphorylation of mTORC1 downstream targets, including eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), p70 S6 ribosomal protein kinase 1 (p70S6K1), and S6 ribosomal protein (S6RP), independently of PI3K/Akt activity.