Altogether, HBx-Tg mice subjected to HFCD exposure expressed HBx-associated NASH phenotypes; in the in vivo assay, it was demonstrated that HBx-expressing hepatocyte-derived PGE2 mediated hepatic MC polarization dysregulation via the mTOR-NPC1-ER stress signaling pathway; and EP4 receptor-targeted intervention rescued HBx-associated NASH mediated by hepatic MC polarization imbalance (Figure 6). The gene discussed is NPC1; the disease is metabolic dysfunction-associated steatohepatitis.