Since nuclear ABL1 is capable of activating and stabilizing endogenous p73 in response to various DNA-damaging agents including ATO [13, 15, 16, 39, 40] and our previous studies demonstrated the involvement of the p73 pathway in the cytostatic and/or cytotoxic effects exerted by PD and/or ATO treatments on AML, CML and MM cells [13, 15, 16], we sought to determine whether p73 is a molecular target of the combined treatment also in TKIs-resistant BCR::ABL1 leukemic cells. Here, BCR is linked to acute myeloid leukemia.