Intriguingly, the results showed that the combinatory regimens yielded enhanced therapeutic efficacies in CML murine models, potentiated effects on CML cells, and triggered positive feedback signal networks involving BCR-ABL, β-catenin, protein phosphatase 2A (PP2A), NFκB and Bruton's tyrosine kinase (BTK), suggesting potential benefits of IM/BOR for CML patients. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.