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. The gene discussed is TSLP; the disease is chronic rhinosinusitis without nasal polyps.