In mouse pro-B BaF3 cells engineered to express the breakpoint cluster region (BCR)-Abl tyrosine kinase fusion, which drives CML, Kesarwani et al. [70] found that DUSP1/MKP-1 along with FBJ osteosarcoma oncogene (Fos) were responsible for resistance to the Abl TKI inhibitor imatinib (Gleevec). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.