Impaired intestinal barrier function promoted by JNK during H/R may therefore also lead to portal vein endotoxemia, activation of TLR4 with phosphorylation of MAPKs, and increased production of inflammatory cytokines and ROS by hepatic Kupffer cells [34, 35, 43, 44]. The gene discussed is TLR4; the disease is serum lipopolysaccharide activity.