Recently, we reported an unanticipated effect of HDAC inhibitors on HIV infection that was independent of its effects on nuclear histones: pre-treatment of primary CD4+ T cells with drugs that inhibited the cytoplasmic HDAC6 enhanced the kinetics and efficiency of reverse transcription, nuclear import, and integration and led to a significant increase in susceptibility to HIV infection [16]. The gene discussed is HDAC6; the disease is HIV infectious disease.