Third, in bone marrow chimeras in vivo, the hyperactive ASXL1–BAP1 complex cooperated with loss of TET2 to promote commitment of haematopoietic cells to the myeloid lineage, consistent with the fact that combined mutations of ASXL1 (encoding truncated versions of ASXL1 protein) and TET2 (encoding loss-of-function mutants) are frequently observed in myeloid disorders46, 47 including MDS, myeloproliferative neoplasms, systemic mastocytosis, chronic myelomonocytic leukemia and acute myeloid leukemia. This evidence concerns the gene BAP1 and chronic myelomonocytic leukemia.