Under normal circumstances, its kinase activity is auto-regulated and maintained at an average level to prevent oncogenic events in leukemia.21 However, constitutively activated BCR-ABL1, a gene fusion product resulting from chromosomal translocation,20 leads to uncontrolled growth and survival of hematopoietic stem cells and initiates CML pathogenesis. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.