A time course study using splenic CD11c+ DCs isolated from CLP mice revealed that the phosphorylation of p65 and IκBα was highest at 24 h after sepsis, in parallel with the activation of TNF receptor-associated factor 2 (TRAF2), which served as a pivotal adaptor in transmitting signals from TNFRSF (Figure 8C-D). The gene discussed is NFKBIA; the disease is Sepsis.