AhR defective signaling contributes to pathogenic responses, witnessed in celiac disease patients, with AhR transcript decreased in IECs and peripheral mononuclear cells, although, an AhR agonist (6-Formylindolo(3,2-b)carbazole; Ficz), reduced pro-inflammatory cytokine, granzyme B and perforin expression in vitro, and reverted intestinal injury in a poly I:C-induced-celiac disease murine model (179). This evidence concerns the gene PRF1 and celiac disease.