CRSwNP is driven predominantly by type-2 inflammation in which epithelial “alarmins” (e.g., TSLP/IL-33) activate dendritic cells and type-2 lymphocytes, leading to downstream IL-4/IL-13/IL-5 signaling that promotes IgE class-switching, eosinophilia, edema, mucus hypersecretion, and olfactory epithelial dysfunction [61]. The gene discussed is IL4; the disease is Increased total eosinophil count.