Some factors previously implicated in the pathogenesis of EoE include allergen-induced cytokines (e.g., IL-5, IL-13, IL-33), epithelial cells, nerve cell-derived chemokines, induction of eotaxin-3 and VIP, and genetic factors15,17,36–40; however, targeting these Th2 cytokines has not yet been shown to successfully block EoE pathogenesis with any clinical significance. Here, CCL26 is linked to eosinophilic esophagitis.