However, Usp18 and IFN receptor R1 (Ifnar1) double deficient bone marrow cells with p210 BCR-ABL transduction reverse the original resistance to CML disease development, which indicates the important role of type 1 IFN signaling in the resistance to CML development in Usp18-deficient bone marrow cells [43]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.