BCR-ABL stabilizes β-catenin in myeloid cells through induction of tyrosine phosphorylation and activation of β-catenin in BCR-ABL-positive granulocyte-macrophage progenitors from blastic phase CML patients facilitates the acquisition by these cells of properties of LSCs [1]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.