The pathogenesis of EGE is unclear, but numerous studies indicated an overproduction of cytokines-secreting T helper type 2 effector cells, chemokines, eotaxin-1, interleukin-5 (IL-5), and interleukin-15, which leads to the upregulation of eosinophils and infiltration of the GI tract causing a cascade of inflammatory response [1,3,5]. This evidence concerns the gene IL5 and eosinophilic gastroenteritis.