IFI16 and infection: Taken together, these observations suggest that: a) KSHV de novo infection increases nuclear H2B acetylation which is subsequently transported to the cytoplasm via Ran-GTP; b) ASC does not play any role in H2B acetylation and its cytoplasmic transportation; and c) IFI16-H2B is an independent complex distinct from the IFI16-ASC-procaspase-1-inflammasome complex formed during KSHV infection.