CD109 expression on T cells may amplify Th2 effector function by inhibiting TβR signal transduction.[52] Since CRSwNP is predominantly driven by type 2 inflammation[2] and AR inflammation is also primarily mediated by Th2 cells,[53] both conditions share similar pathogenic mechanisms related to airway allergic inflammation. The gene discussed is CD109; the disease is chronic rhinosinusitis with nasal polyps.