Activation of p53 by blockade of MDM2 sensitized BC CML cells, including CD34+CD38− and quiescent CD34+ progenitor cells, to TKI- and Bcl-2 inhibitor-induced apoptosis but had very limited toxicity in CD34+ cells from normal BM controls, suggesting a potential for utilizing this strategy in the treatment of BC CML and elimination of quiescent CML stem/progenitor cells. Here, BCL2 is linked to breast cancer.