In Western countries, CRSwNP predominantly manifests eosinophil-dominant type 2 inflammation involving various cytokines (e.g., IL-4, IL-5, IL-13, and IL-33) that regulate the proliferation and differentiation of eosinophils, thereby affecting their transmigration and enhanced survival in the peripheral sinonasal mucosa [4]. This evidence concerns the gene IL33 and chronic rhinosinusitis with nasal polyps.