Furthermore, one would expect that in the presence of a Tat inhibitor, it would be very difficult for external stimuli such as antibodies (αCD3/CD28), or phorbol esters (PMA) or HDAC inhibitors to reactivate virus production from the integrated provirus, as it is known that HIV-1 lacking Tat undergoes some basal transcription; however, it does not sustain a spreading infection [37]. The gene discussed is TAT; the disease is infection.