CXCL16 and cancer: Primary bile acids increase the expression of CXCL16 in liver sinusoidal endothelial cells; however, microorganisms reduce the expression of CXCL16 in hepatic sinusoidal endothelial cells as they convert primary bile acids to secondary bile acids, impairing the immune function of natural killer T cells.[11] In conclusion, the regulation of microbial metabolites has the potential to improve the efficacy of immunotherapy targeting cancer.