Our hypothesis is that, in CML, Aurora kinase A together with PLK1 may cooperate with the constitutively activated BCR::ABL1 tyrosine kinase promoting the occurrence of additional genetic and genomic alterations that may be direct or indirect drivers of TKIs resistance and disease progression to blast crisis (BC). The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.