From this perspective, studies on a comprehensive research model linking IL‐5 levels, ILC2 to ILC1 shift, and the role of IL‐18/IL‐33 production in patients with COPD could provide a more robust support for the hypothesis of a reduced IL‐5‐dependent stimulus on eosinophil entrapment after IL‐4/IL‐13 inhibition [22]. This evidence concerns the gene IL33 and chronic obstructive pulmonary disease.