Unlike resistance mechanisms observed in some other cancers such as imatinib-resistant chronic myeloid leukemia (CML) where the resistant cells often have mutations in the gatekeeper residues in BCRABL which allows the cells to proliferate and activate additional signaling pathways in the presence of imatinib, others mechanism for Raf inhibitor-resistance are more frequently observed in cells containing BRAF mutants. This evidence concerns the gene BRAF and chronic myelogenous leukemia, BCR-ABL1 positive.