AHR and neoplasm: Targeted AhR knockout within intestinal epithelial cells (IECs) (Vil1CREAhRfl/fl) supported ligand- and AhR-dependent regulation of crypt intestinal stem cell differentiation, IEC regeneration, inhibition of pro-inflammatory signaling, and preservation of barrier integrity, while addition of Citrobacter rodentium to IEC-specific AhR−/− resulted in dysregulation of intestinal stem cell proliferation, differentiation, and subsequent increased tumor burden relative to wild-type mice [11].