β-catenin inhibition can therefore reverse TKI resistance in BP-CML cells, either with or without BCR–ABL kinase domain mutations, and has been shown to synergize with TKI both ex vivo and in vivo [80], supporting the potential utility of combined inhibition of β-catenin and BCR-ABL for therapy of CML, particularly TKI-resistant BP-CML. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.