The development of small molecule tyrosine kinase inhibitors (TKI), which effectively interfere with the interaction between the BCR-ABL1 oncoprotein and adenosine triphosphate (ATP) and thus block the proliferation of malignant granulocytes, has revolutionized the field of CML therapy. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.