composed of several chemical elements, some of which have been shown to affect different targets by acting on DNA through epigenetic inuences in the intestinal cells and even by modulating the microbiota in the intestinal lumen [9, 10]. From a clinical perspective, a recent study addressing the impact of smoking in IBD identi­ed an increased risk of surgery among current smokers with CD, while former smokers with UC have an increased risk of colectomy [11]. On the other hand, another recent study involving the Sydney IBD Cohort database conrmed the det­rimental effects of smoking in CD but failed to demonstrate substantial benets from smoking in UC [12]. Interestingly, in a recent study, investigators analyzed the association between cigarette smoking and pancreatic brosis and concluded that aryl hydrocarbon receptor (AhR) ligands found in cigarette smoke increase the severity of pancreatic brosis in an experimental model of chronic pancreatitis in mice through the up-regulation of IL-22. In addition, in humans, higher levels of IL-22 have been identied in serum samples from smokers compared to nonsmok­ers [13]. AhR activation has been shown to deliver anti-inammatory signals dependent on the induction of regulatory T cells [14] and to promote IL-22 produc­tion by Th17, Th22 and gamma-delta T cells [15]. In the context of CD, the low expression of AhR found in lamina propria mononuclear cells [16] has recently been associated with elevated levels of Smad7, an inhibitor of transforming growth factor beta 1 (TGF-beta 1) activity, which in turn regulates AhR expression [17]. Although the exact mechanism by which smoking affects mucosal immunity is yet to be determined, abnormal signaling mediated by AhR may represent a potential link between the environment and the consequences of inammation, including brogenesis.