a complex process with a wide variety of clinical, genetic, epigenetic, and environ­mental risk factors. Originally thought to be a consequence of chronic inamma­tion, new evidence arises for non-inammatory contributors to stricture formation, suggesting an intricate interplay of cellular, molecular, and additional host/environ­mental factors. Although no specic medical treatments for brostenotic intestinal strictures currently exist, understanding the molecular pathways involved in stric­ture formation will undoubtedly guide therapeutic developments. As mediators of inammation and immunoregulation, cytokines are key effectors in the brotic pro­cess. Accordingly, targeting inammation, in part via cytokine blockade, has been the mainstay of therapy in IBD.In many cases, inammatory disease is associated with signicant brotic change, as increased inammation perpetuates the cascade of mucosal repair. Thus, inammatory cytokine-targeted therapy may serve as one potential avenue for treating brostenosis. As regulatory and repair mechanisms have been implicated in brosis as well, either as sequelae of inammation or via de novo pathways, a parallel route for treating intestinal brosis may be the targeting of “regulatory” cytokines. This chapter will highlight the relevant contributions and potential therapeutic targeting of cytokines involved in inammatory and regulatory pathways leading to brosis.