To definitively implicate TLR4 in CR-induced NF-κB activation, we utilized Tlr4−/− mice in the B6 background wherein, initial kinetics of NF-κB activation at day 3 highlighted the need for the presence of TLR4; NF-κB activation at day 5 however, may represent a homeostatic response to counter bacterial infection while NF-κB activation at day 12 which correlated with peak hyperplasia (see Fig. 1) may represent an intrinsic pathway activation independent of TLR4. The gene discussed is TLR4; the disease is bacterial infectious disease.