CRS engages the innate immune system, does not necessitate antibody formation, and can manifest upon initial exposure [6]; these agents induce CRS by prompting the rapid release of tumor necrosis factor (TNF)-α and interferon (IFN)-γ, succeeded by a subsequent release of interleukin (IL)-6, resulting in the extensive activation of several inflammatory mediators [7]. The gene discussed is IFNG; the disease is congenital rubella syndrome.