Inflammatory bowel disease (IBD) is a medical condition that predominantly affects the gastrointestinal tract (48) . De Jager et al. showed that TLR4 and its signaling molecule TIRAP affect susceptibility to IBD (49) . Recent studies have shown that TLR4 −/− and MyD88 −/− knockout mice tend to be more prone to severe dextran sulfate sodium-induced colitis than their wild-type littermates (50) . Interestingly, CRX-526 a TLR4 antagonist has been shown to prevent an inflammatory disease in the dextran sulfate sodium and mdr1a −/− /1b −/− deficient mice models (51) . To explain these contradictory results we have to consider that constitutive signaling through TLR4 may result in the production of tissue protective factors such as IL-6 and TNF-α (49) . This is the scenario in the MyD88 −/− knockout mice, while in the case of the CRX-526 we may have selective downregulation of one of the TLR-4/ LPS signaling pathways.