Previous work has indicated that the HDAC inhibitors vorinostat (suberoylanilide hydroxamic acid, SAHA; marketed as Zolinza for the treatment of cutaneous T cell lymphoma) and panobinostat (LBH-589; currently in Phase III trials for cutaneous T cell lymphoma) successfully alleviate the NPC phenotype in NPC mutant cells [14]. The gene discussed is HDAC9; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.