Alternatively, changes in the heterodimer regulatory complex (IL22RA1-IL10R2, IL20, and IL24) could lead to decrease in the innate immune response (β-defensins, mucins and metalloproteinases), increased levels of pro-inflammatory cytokines (IL-6, IL-8, and TNF), and reduced apoptosis,3, 4 providing other possible pathophysiological mechanisms involved in the development of CRS. The gene discussed is IL22RA1; the disease is congenital rubella syndrome.