For example, although TET2 and ASXL1 mutations may be independent drivers of CMML in some patients [3], combined mutations of TET2 and SRSF2 and of ASXL1 with SETBP1 are consistent with a two-step ‘linear’ model of CMML development [14]. This evidence concerns the gene TET2 and chronic myelomonocytic leukemia.