CRS is a supraphysiologic inflammatory state triggered by inflammatory cytokines and chemokines, including interferon (IFN)-y and tumor necrosis factor (TNF)-a, released by CAR T cells after engaging with the target antigen CD19; resultant activation of bystander host antigen-presenting cells (APCs) and T cells has been shown to be the primary source of IL-6 and IL-1, both identified as key drivers of CRS [23,85]. This evidence concerns the gene IL6 and congenital rubella syndrome.