In atypical CML, lacking the BCR/ABL fusion, recurrent SETBP1 mutations are found in 17/70 cases, some of which abrogate a site for ubiquitination, resulting in increased amounts of SETBP1 and SET protein, lower PP2A activity, and higher proliferation rates (136). This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.