TAT and infection: We show here that, small molecules such as GNE049 or JQ1 can remove the enhancer functionality of the provirus, so that when the T cell is activated, HIV-1 latency reversal within the H3K4me1 compartment of the reservoir is Tat-independent, and thus unable to contribute to new infections but still producing cytotoxic viral proteins and potentially exposing the cell to the immune system for elimination.