The clinical implementation of tyrosine kinase inhibitors (TKIs) over a decade ago has revolutionized treatment of chronic myeloid leukemia (CML) but the occurrence of resistance, most commonly attributable to point mutations in the tyrosine kinase domain (TKD) of the BCR-ABL1 fusion gene, remains an important challenge [1,2,3,4,5]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.