CHB typically exhibits portal inflammation, while NAFLD manifests macrovesicular or mixed macrovesicular steatosis, primarily in the acinar zone 3, along with or without hepatocyte ballooning, mixed lobular inflammatory cell infiltration, and perisinusoidal fibrosis.10 Studies highlight significant interconnection between the HBV virus molecules and major NAFLD pathways; for instance, liver steatosis may relate to HBV-X protein and farnesoid X receptor.22 However, the impact of HBV infection on NAFLD occurrence or vice versa remains uncertain. This evidence concerns the gene NR1H4 and metabolic dysfunction-associated steatotic liver disease.