It has been suggested that the HBV-X protein produced by HBV in hepatocytes can transactivate the Galectin-3 promoter or upregulate Galectin-3 expression through the CREB/ATF-transcription pathway after HBV infection, and this phenomenon is more obvious in normal liver cells than in hepatoma cells (23). Here, LGALS3 is linked to hepatocellular carcinoma.