In conclusion, TH2 cytokines IL-4, IL-5, and IL-13 not only contribute to CRS inflammation by rupturing the epithelial barrier, mediating the cilia dysfunction and mucus production, mediating altered nasal mucosal macrophage function, reducing innate immune function in the nasal cavity stimulating the development of mucosal edema and pseudocysts (57), but can also display strong pro-fibrotic properties. The gene discussed is IL13; the disease is congenital rubella syndrome.