Given that S100A9 functions as a ligand for TLR4 [68], and that TLR4 and CHI3L1 signaling pathways are interconnected in inflammatory bowel diseases [69], the ability of Fh15 to suppress both S100A9 and CHI3L1 suggests that it may also modulate additional molecules involved in these associated signaling pathways. This evidence concerns the gene CHI3L1 and inflammatory bowel disease.