Jamieson et al. [75] reported that during blast-crisis of chronic myelogenous leukemia (CML), granulocyte-macrophage progenitors acquired much stronger self-renewal property due to the activation of Wnt/β-catenin pathway, and expressed BCR-ABL protein and expanded imatinib-resistant CML. Here, BCR is linked to chronic myelogenous leukemia, BCR-ABL1 positive.