(33) However, studies from a fully immunocompetent mouse model demonstrated that treatment with IFN-ɣ knockout CAR T cells resulted in similar levels of proinflammatory cytokine elevation and occurrence of clinical CRS in the treated mice compared to those treated with the wild-type CAR T. While possible that IFN-ɣ signaling plays a more significant role in humans compared to mice, these results suggest that in vivo IFN-ɣ signaling may be redundant or not directly causal for CRS development (34). The gene discussed is IFNA1; the disease is congenital rubella syndrome.