While it was reported in the literature that expression of SOCS proteins can be induced upon stimulation with IFN [61] we could not detect any significant gene induction by IFNb in A549 cells. Instead we observed a significant up-regulation of SOCS-3 by viral 59 triphosphate RNA, indicating that gene induction occurs via accumulation of vRNA during infection. This appears to occur through the RNA-mediated activation of the IKK/NF-kB pathway, most likely activated through engagement of the RNA sensor RIG-I. At a first sight, this might appear controversial since NF-kB activation is among the RIG-I-induced signaling responses and NS1 was reported to inhibit this signaling pathway. However, despite the action of NS1 it is well known that NF-kB is still significantly activated upon influenza virus infection and many NF-kB and IFNb dependent genes are still expressed. We hypothesized previously that the incomplete inhibition conferred by NS1 is an indication that the virus exploits the remaining signaling activities for efficient replication [52, 62, 63] . The findings described here, namely NF-kB dependent induction of SOCS-3 and limitation of type I IFN signaling responses, provide yet another example how influenza viruses take advantage of NF-kB activity.