Overexpressions of TNFRSF18, IL2RA, and INHBB in either ECRS or Asp groups may also reflect the disease severity and pathology of the CRSwNP phenotype via interference of cytokine–cytokine receptor interaction despite poor reports of pathological analyses between the overexpressions of these genes and the phenotype of ECRS and/or Asp. This evidence concerns the gene INHBB and chronic rhinosinusitis with nasal polyps.