As it has been demonstrated that the BCR-ABL protein can establish β-catenin expression in CML via TK-mediated phosphorylation [47], this finding suggests that in drug resistance in CML, the canonical Wnt pathway could be more strongly activated to positively regulate ABCB1 transcription, as previously evidenced in other types of cancer. Here, ABCB1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.