This included disruption of the epithelial barrier (AMPK [42], MAPK [43], and HIF-1α signaling [44]); inflammation (Wnt signaling [45]); fibrosis (TGF-β signaling [46]), which is particularly pronounced in untreated EoE patients [47]; and eosinophil degranulation (Th17 cell differentiation [48]). Here, HIF1A is linked to eosinophilic esophagitis.