Interestingly, we observed a further increase of mCherry fluorescence in VprWT-infected cells treated with HDACi (Figure 6H), suggesting that HDAC antagonism is not the primary mechanism through which Vpr modulates the epigenetic landscape during acute infection, even though Vpr-induced histone marks are sensitive to HDACi treatment (Figure S4C). The gene discussed is HDAC9; the disease is infection.