Consistently, we found that intermediate levels of NS1 were sufficient to block the release of pro-inflammatory cytokines in reporter cells, where the supernatant from both IAV-WT and IAV-NS1-T infections failed to induce detectable activity for both NF-kB-dependent alkaline phosphatase and IFN-dependent luciferase reporters (Figure 3D). This evidence concerns the gene NFKB1 and infection.