CXCL16 and hepatocellular carcinoma: Primary (e.g., CDCA, taurocholic acid [TCA]) and secondary (e.g., UDCA, glycolithocholate [GLCA]) bile acids exhibit dichotomous, tissue-specific effects: in the liver, gut microbiota-driven bile acid metabolism controls the CXCL16-CXCR6 axis—CDCA and TCA (≥200 nM) upregulate CXCL16 on liver sinusoidal endothelial cells to recruit CXCR6+ NKT cells and suppress HCC growth, while secondary GLCA antagonizes this by reducing CXCL16 transcription (79).