To investigate whether eIF4Ai may be beneficial to rescue the poor response to therapy driven by mTORC1 activity, we performed studies in the chemoresistant human MOLM-14 model, harboring a KMT2A/MLLT3 fusion but also a FLT3-ITD mutation that constitutively activates mTORC1 signaling, which was established from the peripheral blood of a patient at relapse of AML [12, 49]. The gene discussed is FLT3; the disease is acute myeloid leukemia.