Multiple cytokines and signaling pathways have been implicated in the pathogenesis and progression of CRS including Interleukin (IL)6; IL1; Interferon gamma (IFN-g); and Tumor Necrosis Factor-alpha (TNF-α), with IL6, IL1, and nitric oxide (NO) derived from activated macrophages being considered the central mediators of severe presentations [36,37,38,39]. Here, IFNG is linked to congenital rubella syndrome.