Therefore, we assumed that the inflammatory microenvironment in the nasal polyps prompted the secretion of S100A4 from inflammatory cells, and over-accumulated S100A4 in the tissues would dissociate and enter into peripheral blood as soluble form, resulting in higher serum concentrations of S100A4 in patients with CRSwNP, especially in patients with Eos CRSwNP. This evidence concerns the gene S100A4 and chronic rhinosinusitis with nasal polyps.