Under latency conditions, the HIV provirus is positioned in close proximity to PML nuclear bodies. PML recruits the methyltransferase G9a to the HIV promoter leading to dimethylation of lysine 9 in histone H3 and transcriptional silencing. Upon treatment with the phorbol ester TPA, the deacetylase inhibitor SAHA or arsenic trioxide, a compound inducing PML degradation, the HIV provirus is relocated away from PML nuclear bodies, and HIV transcription is activated.