Figure 12. Schematic diagram depicting the role of XIAP in HFD-induced steatohepatitis. In response to a prolonged challenge with fat-rich diet ingestion, enhanced oxidative stress injury caused by circulatory free fatty acid promotes NLRP3 inflammasome mediated inflammation infiltration, followed by generation of down-stream pro-inflammatory cytokines, ultimately facilitates metabolic disorder associated lipid accumulation in liver. In contrast, activated XIAP and Nrf2 activity are associated with decreased oxidative stress. Circulatory free fatty acid may suppress XIAP expression, further reduce Nrf2 pathway activation. Up-regulation of XIAP may act as the upstream to inhibit ROS generation and induce Nrf2 and other antioxidants activity. In addition, elevated Nrf2 activity and down-stream anti-oxidants including HO-1, NQO-1, SOD or GST further inhibit inflammatory response, finally relieve lipid deposition in liver and hepatic inflammation.