Although vorinostat, an inhibitor of class I and class II HDACs, is effective both in animal models and patients 142-144, treatment with an HDACi with potency against HDAC11, including trichostatin A or panobinostat, was reported to accelerate GVHD by increasing proinflammatory cytokine production 145, 146. Here, HDAC11 is linked to graft versus host disease.