For gut microflora related to individual patient immune status, Kale et al. demonstrated that ‘small’ intestinal immunopathology played a ‘big’ role in lethal CRS in a mouse model.48 Furthermore, they found that IFN-γ-JAK/STAT-driven pathways and IL-17α deficiency contributed to lethal small intestinal immunopathology in T cell-driven CRS. The gene discussed is SOAT1; the disease is congenital rubella syndrome.