Induction of intracellular H3/H4 histone acetylation was observed in all tefinostat-responsive AML and CMML patient samples in contrast to previous studies where other agents such as entinostat, vorinostat and panabinostat induced only modest levels of H3/H4 acetylation and monocytic populations were found to be resistant to HDAC inhibitory treatment [23], [30], [31]. Here, HDAC9 is linked to acute myeloid leukemia.