On the molecular level, the initial trigger for CRS induced by these biotherapies and cellular therapies involves the activation of adaptive immune cells, most often CD4+ and CD8+ T cells, which leads to a release of proinflammatory mediators by these cells such as interferon gamma (IFN-γ), interleukin (IL-2), and tumour necrosis factor alpha (TNF-α) (10, 11). The gene discussed is IFNG; the disease is congenital rubella syndrome.