The pathogenesis of EoE is most likely a mixed IgE and non-IgE/cell mediated food reaction, in which Th2 cytokines, particularly thymic stromal lymphopoietin (TSLP), interleukin (IL)-4, IL5, IL13, and transforming growth factor-β (TGF-β), and eosinophilic chemokines (eotaxin 1-3/CCL11-CCL24-CCL26 and RANTES/CCL5) play a central role in eosinophilic recruitment, perpetuating local Th2-inflammation. The gene discussed is CCL5; the disease is eosinophilic esophagitis.