Pertaining to the involvement of inhalants in the pathogenesis of EoE, an experimental study in rats using a placebo control demonstrated that esophageal hypersensitivity was simultaneous with the development of pulmonary inflammation, particularly in genetically modified animals that were eotaxin-3 and interleukin 5-positive, demonstrating that similar to asthma, sensitivity to inhalants might be involved in the pathogenesis of the disease [30]. The gene discussed is CCL26; the disease is asthma.