We therefore hypothesized that depletion of glutamine induced by PegC would not only inhibit proliferation of CK-AML but also enhance the anti-apoptotic activity of Ven-mediated antagonism of BCL-2 in CK-AML by decreasing the expression of proteins such as MCL-1, whose translation is dependent on eukaryotic translation initiation factor 4E (eIF4E)- eIF4E-binding protein (4EBP1) interaction. The gene discussed is EIF4E; the disease is acute myeloid leukemia.