CRSsNP may benefit from therapies aimed at inhibiting TGF-β1 signaling and fibroblast activity to reduce fibrotic tissue accumulation, while CRSwNP may require interventions targeting epithelial cytokines (e.g., TSLP, IL-4, and IL-13), vascular remodeling, or basal cell dysregulation. Here, IL4 is linked to chronic rhinosinusitis without nasal polyps.