IFNG and chronic rhinosinusitis without nasal polyps: While Th2-dominant inflammation, driven by cytokines such as IL-4, IL-5, and IL-13, is well established in eosinophilic CRSwNP, recent work has highlighted the importance of Th1 (e.g., IFN-γ) and Th17 (e.g., IL-17A, IL-22) pathways in CRSsNP and in neutrophilic or mixed inflammatory phenotypes of CRSwNP [2,3].