Impaired barrier function allows pathogenic microorganisms to stimulate nasal mucosal epithelial cells to produce inflammatory mediators, activating and recruiting various immune and inflammatory cells, including eosinophils, thus triggering an inflammatory cascade, and exacerbating histopathological changes in CRSwNP.35, 36 The expressions of systemic inflammation biomarkers, such as CRP, fibrinogen, IL-6, and TNF-α, were found to be enhanced in the serum of MetS patients.37 The gene discussed is CRP; the disease is chronic rhinosinusitis with nasal polyps.