In addition, it was found that FGL2 could induce activation of NF-κB and MAPK signaling pathways in LPS-induced macrophages, which have been proved to be activated in IBD [26] Moreover, miR-146b and FGL2 were overexpressed in macrophages, and it was found that miR-146b overexpression reduced inflammation and M1 phenotypes of macrophages, which was rescued by FGL2 upregulation, suggesting that miR-146b acted as an inhibitor in inflammation response and M1 macrophage polarization in an FGL2-dependent manner. Here, FGL2 is linked to inflammatory bowel disease.