The BCR-ABLfusion leads to activation of ABL kinase, which is a major, maybesufficient, driver for disease development.3 Kinase inhibition with imatinib (Gleevec) has become the standardtherapy for CML.4 The second and thirdgeneration inhibitor in combination with the allosteric inhibitorasciminib constitute the newest line of therapy largely preventingrecurrence through resistance mutations in BCR-ABL.5 The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.