FGL2 and metabolic dysfunction-associated steatohepatitis: In this study, we reveal a novel pathologic mechanism by which fgl2 expressed by macrophages upregulates the NF-κB and p38-MAPK signaling pathways and NLRP3 inflammasome, resulting in overproduction of proinflammatory cytokines and ROS, which leads to hepatic lipid metabolism disorders and severe liver injury in NASH (Figure 9).