Despite the significant increase in life expectancy of CML patients due to the development of BCR-ABL-targeting tyrosine kinase inhibitors (TKIs) [1], a quarter of patients will fail TKI therapy due to BCR-ABL kinase mutations, alternative oncogene activation, or because of progression to accelerated phase or blast crisis [2]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.