LSCs have aberrant regulation of beta-catenin, and in a CML murine model BCR/ABL1 seems to stimulate beta-catenin through the phosphoinositide 3-kinase (PI3K/AKT) signaling, then increasing the leukemic progression (15). This evidence concerns the gene CTNNB1 and chronic myelogenous leukemia, BCR-ABL1 positive.