Because the BCR-ABL kinase inhibitor imatinib has an initial therapeutic effect but does not eliminate LSCs in CML mice [7], [17], we reasoned that the failure of imatinib to cure CML mice should be associated with an inability of imatinib to cause an increase in the transition of LSCs to LSK− cells in CML mice treated for a long period of time. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.