While we cannot completely exclude the possibility that Nmi may affect the IFN-γ responses by interacting with HCMV proteins other than UL23, our results in experiments expressing UL23 alone in the absence of HCMV infection and in experiments using anti-Nmi siRNA and UL23-deficient mutants suggest that UL23 may interact with Nmi and affect its cellular localization and interactions with STAT1 in the absence of other HCMV proteins, possibly leading to the inhibition of IFN-γ induced STAT1-dependent transcription. This evidence concerns the gene RPL23A and cytomegalovirus infection.