While eosinophilia associated with dupilumab is prominent in asthma, CRSwNP, and AD, its absence in COPD and EoE patients underscores the need for targeted experimental studies to validate the hypothesized involvement of alternative inflammatory pathways, such as IL‐18 and IL‐33 signaling, as well as the role of ILC2 plasticity. The gene discussed is IL18; the disease is eosinophilic esophagitis.