We have found that, in imatinib-resistant CML cell lines, without BCR-ABL1 mutations, CK2 differently potentiates the resistant phenotype, either by overexpressing its protein-level [17] or by a BCR-ABL-independent activation of rpS6 [16]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.