Histone deacetylase (HDAC) enzymes have been implicated in both normal physiology and pathophysiology, and several HDAC inhibitors have entered clinical trials.1, 2, 3 These inhibitors include vorinostat, a direct-acting compound that fits the HDAC active site, and romidepsin, a prodrug that through reductive metabolism generates a zinc-binding thiol.4 Evaluation of such compounds against solid tumors and hematological malignancies has provided insights into clinical efficacy, as well as resistance mechanisms and off-target effects.1, 2, 3. Here, HDAC9 is linked to hematologic disorder.