BCR-ABL1 is a hallmark of chronic myeloid leukemia (CML), which therapy has been revolutionized by imatinib, a tyrosine kinase inhibitor (TKI), which has changed CML from a fatal disorder into a chronic disease.1 Imatinib binds the adenosine triphosphate (ATP)-binding pocket in BCR/ABL1, inhibiting its kinase activity by blocking its binding by ATP, its cofactor. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.