Furthermore, CD109 can attenuate epithelial-mesenchymal transition in human nasal epithelial cells by inhibiting the TGF-β1/Smad signaling pathway, thereby suppressing epithelial-mesenchymal transition.[41] Zhang JM et al found that CD109 not only weakened TGF-β1 signaling in human glioblastoma cells but also enhanced EGF signaling.[42] Additionally, CD109 influences the postoperative recurrence of recurrent CRSwNP.[34] The present study further confirms the potential of CD109 as a diagnostic marker for CRSwNP. Here, EGF is linked to glioblastoma.