The liver functions as a firewall to filter out the commensal bacteria and their products.23 However, this function is attenuated in CLD,23,24 making increased bacterial translocation, a hallmark of CLD, which not only contributes to characteristic infectious complications but also generates a chronic inflammatory state in the liver.25 Among all the PAMPs/PRR signaling pathways, the role of lipopolysaccharide (LPS)/TLR4 signaling in CLDs has been emphasized by many studies. This evidence concerns the gene TLR4 and congenital secretory chloride diarrhea 1.