Historically, MCs have been associated with allergic inflammation, during which their activation plays a critical role in driving type-2 inflammatory diseases, such as eosinophilic asthma, atopic dermatitis, and eosinophilic gastrointestinal diseases.1 Activation of MCs by crosslinking the FcεRI via IgE induces rapid degranulation and the release of preformed mediators, such as histamine, tumor necrosis factor (TNF), and proteases, as well as the subsequent release of de novo synthesized lipid mediators, cytokines, and chemokines. The gene discussed is TNF; the disease is eosinophilic gastrointestinal disease.