Previously, our group has shown that RSV infection in mice and infants promotes IL-1β pathway activation, which leads to the induction of innate cytokines (CCL2, TSLP and IL-33) by the airway epithelium [12] and that the inhibition of the IL-1β pathway with IL-1 receptor antagonist during early-life RSV infection altered RSV immunopathology and diminished subsequent exacerbated allergic disease [13]. The gene discussed is IL1B; the disease is allergic disease.