This is consistent with our finding that NOD2-mediated synergistic induction of IFNβ in response to intracellular bacterial infection was only manifest when TLR signaling was pharmacologically suppressed, and may also explain the results of a previous study in which rip2−/− macrophages with intact TLR signaling had no defect in their response to L. monocytogenes [37]. This evidence concerns the gene NOD2 and bacterial infectious disease.