Our work clearly demonstrates that EIF4A2 is more highly expressed in LSCs and is required to support the proliferation, survival and undifferentiated state of AML cells, indicating the RBM17/EIF4A2 axis we have uncovered is indeed targetable for AML treatment and that the inhibitory nature of rocaglamide on AML function is likely due largely to its effects on EIF4A2. Here, EIF4A2 is linked to acute myeloid leukemia.