Therefore, we used the purified SAg to induce CRS in HLA-DR3 transgenic mice to delineate the roles of IFN-γ and IL-17A, the signature pro-inflammatory cytokines produced by activated CD4+ and CD8+ T cells, in the immunopathogenesis of CRS and validated a JAK-1/2 inhibitor, ruxolitinib for the treatment of CRS. This evidence concerns the gene JAK1 and congenital rubella syndrome.