This is associated with release of several cytokines such as interferon-γ (IFN-γ) and tumor-necrosis factor α (TNF-α).20 Second, the combination of these signals triggers the activation of monocytes and macrophages with enhanced tumoricidal capacity.21 The activated macrophages secrete high levels of pro-inflammatory cytokines (IL-6, IL-1, IL-10)21 and other mediators such us inducible nitric oxide synthase (iNOS),22 resulting in progression of CRS. This evidence concerns the gene TNF and congenital rubella syndrome.