Based on our findings, we propose that combined targeting of Aurora kinase A or PLK1+WEE1 may be an excellent strategy for inducing apoptosis in CML cells whose resistance is driven by BCR::ABL1-independent mechanisms, or where all TKIs have failed, including advanced stages of CML. This evidence concerns the gene PLK1 and chronic myelogenous leukemia, BCR-ABL1 positive.