In addition, the PirB/LILRB2-ANGPTL8 interaction induces the proinflammatory phenotype and stimulates cytokine production in the liver via activating the P38, AKT, and NF-κB signaling pathways, which in turn causes an aggravation in hepatocyte lipid accumulation and an exacerbation from simple steatosis to steatohepatitis (Fig. 7). Here, AKT1 is linked to steatosis.