Investigations have demonstrated that inappropriate regulation of TLR2 and TLR4 signaling caused inflammatory responses in CRS.30, 31 The LPS/TLR4 signaling pathway is divided into two transduction pathways, the one is MyD88-dependent response pathway, which mediates the release of proinflammatory cytokines IL-1β, IL-6, IL-8 and TNF-α; the second is non-MyD88-dependent response pathway, which activates NF-κB and mediates the secretion of type I interferon.32 This evidence concerns the gene TLR2 and congenital rubella syndrome.