There is an increasing body of evidence that suggests that EoE is driven by food and aero‐allergen exposure,3, 4, 5 resulting in the activation of interleukins (IL)‐5, IL‐13 and IL‐33, subsequently promoting eosinophil migration into and activation in the oesophagus, ultimately leading to oesophageal remodelling.4, 6, 7. This evidence concerns the gene IL5 and eosinophilic esophagitis.