Recently it was reported that IFN-induced gene expression responses are potentiated in cells, which lack the NF-kB factors p50 or p65 [64] . Although these authors described an inhibitory binding of NF-kB transcription factors to some IFN-induced gene, this mechanism might be cell type dependent since we could not observe similar effects in the cell types used here (data not shown). Thus, the underlying molecular mechanisms appear to be not fully clear. It is striking that the effects described for p50 and p65 knock out cells in these studies fully correlate with our observations in SOCS-3 deficient cells. While in the latter case cells lack the IFNb signaling inhibitor SOCS-3, the p50 and p65 knock out cells are deficient for the factors required for SOCS-3 induction. Thus, given the NF-kB dependent induction of SOCS-3 described in the present manuscript, we provide an additional molecular mechanism that may explain the phenomenon described by Wei et al. [64] .