We previously reported that FLT3-ITD activates the mTORC1/S6K/4EBP1 pathway cooperatively through the STAT5/PIM and PI3K/AKT pathways in AML cells, which promotes proliferation and survival, as well as therapy resistance to PI3K/AKT inhibitors and proteasome inhibitors, at least partly, by upregulating cap-dependent translation by the eIF4F complex [12,13,14]. This evidence concerns the gene FLT3 and acute myeloid leukemia.