TGFβ1 treatment activates Smad signalling, resulting in (1) the overexpression of EMT-related genes [51], (2) increased production of collagen and connective tissue growth factor (CTGF) [5], (3) enhanced migratory and contraction capacities [6], (4) formation of myofibroblasts, particularly in the pedicle area of nasal polyps, and (5) accumulation of fibronectin, which is significantly elevated in CRSwNP patients compared to controls [52,53,54]. Here, CCN2 is linked to chronic rhinosinusitis with nasal polyps.