EoE shares several commonalities with asthma, including aberrant eosinophil activation and recruitment, the prominence of IL-13 and epithelial dysfunction, and overlapping therapeutic targets such as the IL-4 receptor, IL-13, thymic stromal lymphopoietin, IL-5, and IL-5R [98, 99]. This evidence concerns the gene IL5 and eosinophilic esophagitis.