For example, non-allergic asthma and nasal polyposis are driven by an intricate interplay of innate immune cell subsets, including ILC, macrophages, eosinophils and neutrophils53,173–175, which may have undergone long-term reprogramming in response to pathological triggers such as viral or bacterial infection or exposure to pollutants or molds93,176–178. This evidence concerns the gene CCL27 and Nasal polyposis.