Indeed, by leveraging on the capability of the MEKi to promote normal ABL1 nuclear translocation, the subcellular compartment where it can exert its tumor suppressor functions, we could also demonstrate here that the allosteric activation of nuclear ABL1 kinase activity by DPH significantly potentiates the anti-leukemic effects of the MEKi Mirdametinib on model leukemic cell lines and patient-derived leukemic blasts. Here, ABL1 is linked to neoplasm.