While this is likely due in part to low, almost undetectable levels of Tat co-factor Cyclin T1 in monocytes [61], Cyclin T1 protein being induced upon HIV-1 infection of macrophages [62], a modest increase in protein levels following nucleofection of pCyclin T1 cannot restore Tat transactivation [60], suggesting additional blocks to transcription (and/or a very high limiting level of Cyclin T1 in monocytes). The gene discussed is TAT; the disease is HIV-1 infection.