With this rationale in mind, we compared the inhibitory capability of the recently developed BTK inhibitor Ibrutinib and the PI3Kδ inhibitor Idelalisib against the NVP-BEZ235, a dual PI3K/mTOR kinase inhibitor that has demonstrated ability to attenuate both 4E-BP1 phosphorylation and eIF4G activity in AML [23, 69-71]. The gene discussed is EIF4G1; the disease is acute myeloid leukemia.