These findings are consistent with the notion that TLR4 down-regulation is important for the resolution of inflammation and repair of membrane damage, as established by previous studies showing that TLR4 knockout mice had reduced inflammation in response to pathogen infection [39], and that TLR4 antagonist inhibited pro-inflammatory cytokine production and mucosal damages in dextran sodium sulfate-induced colitis mice and in spontaneous chronic colitis model [40]. The gene discussed is TLR4; the disease is infection.