More recently, Cbl mutations that disrupt E3 function have been found in ~5% of a wide variety of myeloid neoplasms including myelodysplastic syndrome, myelofibrosis, refractory anemia with excess blasts, de novo and secondary acute myeloid leukemia (AML and sAML, respectively), atypical chronic myelogenous leukemia (aCML), CML in blast crisis, chronic myelomonocytic leukemia (CMML), and juvenile myelomonocytic leukemia (JMML) (reviewed in [12]). This evidence concerns the gene CBL and chronic myelogenous leukemia, BCR-ABL1 positive.