As a result, the fusion oncogene, BCR-ABL1 is formed and translated into a constitutively active tyrosine kinase, which plays an essential role in the pathogenesis of the disease.1,2 Inhibition of BCR-ABL1 activity by long-term administration of imatinib or other specific tyrosine kinase inhibitors (TKIs) has revolutionized the treatment of CML. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.