For instance, production by the gut microbiome of a particular secondary bile acid, 3β-hydrodeoxycholic acid, has been demonstrated recently to act via FXR to promote the generation of peripheral regulatory T cells,86 but the potential implications of this and other bile acid-immune interactions for CDI (and/or other gut inflammatory disorders) are currently of unclear significance. The gene discussed is NR1H4; the disease is clostridium difficile infection.