The upregulation of primary BA levels and downregulation of secondary BAs have been reported in inflammatory bowel disease (IBD), primarily via the suppression of nuclear factor Kappa-light-chain-enhancer of activated B cells (NF-κB) via the Farnesoid X receptor (FXR) and Pregnane X receptor (PXR) activation [106,107,108]. Here, NR1H4 is linked to inflammatory bowel disease.