The effective in vitro targeting of HDAC inhibition in monocytoid AML and CMML described above, combined with encouraging early signs of clinical activity (coupled to selective HDAC inhibition) in the absence of tefinostat-related toxicity in the Ossenkoppele study, provides a compelling case for further clinical evaluation of tefinostat in larger studies in monocytoid-lineage leukaemias. Here, HDAC9 is linked to chronic myelomonocytic leukemia.