Giavridis et al. demonstrated that CRS severity was mediated not by CAR-T-cell-derived cytokines but by IL-6, IL-1, and nitric oxide (NO) produced by recipient macrophages (especially in the mouse peritoneum).27 Furthermore, they concluded that myeloid activation required proximity between CAR-T cells (CD40L) and macrophages (CD40), and indirect cytokine contact. The gene discussed is IL6; the disease is congenital rubella syndrome.