Significant differential expression in 70 genes in nasal cells, including IL13, IL5, periostin (POSTN), calcium-activated chloride channel regulator 1 (CLCA1), and serpin peptidase inhibitor, clade B (SERPINB2), was found to be linked to airway remodeling, production of mucus, and shifting of the immune response toward the Th2 phenotype thus enhancing asthma exacerbation [67, 68]. The gene discussed is POSTN; the disease is asthma.