Based on the different release patterns of activin A, follistatin and TGF-β1, an imbalance between pro-fibrotic (activin A, TGF-β1) and anti-fibrotic (follistatin) mediators was revealed, which favors fibrosis in CRSsNP and edema in CRSwNP. This evidence concerns the gene FST and chronic rhinosinusitis without nasal polyps.