In contrast, OLFM4 knockdown alone was able to abrogate LTC-ICs and no synergistic action was observed between OLFM4 knockdown and imatinib treatment, thereby suggesting that OLFM4-mediated survival of the most primitive CML cells may not depend on BCR-ABL tyrosine kinase-mediated signaling. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.