To determine whether TAK1 is essential to LTB4 to potentiate NOD2-mediated response to IAV infection, we have pretreated mouse embryonic fibroblasts (MEFs) isolated from WT mice with TAK1 inhibitor prior infection with IAV and treatment with LTB4, and measured levels of phosphorylation of IRF3, IRF7 and translocation of NF-κB p65 subunit. This evidence concerns the gene NOD2 and infection.