Given the importance of Muc2 production by goblet cells, particularly as it relates to colitis, we wanted to determine, based on our previous findings, if Muc2 production was directly regulated by AhR, the result of indirect effects, such as the alteration of goblet cell development and proliferation capabilities or even consequential response of IECs to increased IL-22 [15,16]. This evidence concerns the gene AHR and colitis.