To better understand the role of PLK1 and Aurora kinase A in sustaining proliferation of CML cells, we performed clonogenic assays in imatinib-sensitive (K562S) and imatinib-resistant (K562R) K562 cells in the presence of danusertib or volasertib (that inhibit Aurora kinase A and PLK1, respectively). This evidence concerns the gene AURKA and chronic myelogenous leukemia, BCR-ABL1 positive.