NO is crucial in predominantly atopic airway inflammation as a mediator and regulator of lower airway inflammation.23 Inducible nitric oxide synthase (iNOS), responsible for upregulating NO, is also elevated in gastrointestinal diseases such as Inflammatory Bowel Disease (IBD).24–26 Therefore, we hypothesized that increased FeNO may also be observed in patients with active EoE. This evidence concerns the gene NOS2 and gastrointestinal disease.