The potential of the nuclear receptors FXR, PXR, and PPAR-γ as therapeutic targets for IBD has been recently reviewed by Ning et al. [73], and several chemical agents already in clinical use for other diseases have been found to regulate inflammation and tissue repair in IBD via MR activation, such as rosiglitazone and pioglitazone through PPAR-γ, and rifaximin and rifampicin though PXR. This evidence concerns the gene NR1I2 and inflammatory bowel disease.