Specifically, we found that IFNAR1 signaling in the absence of IFNAR2 (Ifnar2−/− mice) was sufficient to prevent the increased BSI susceptibility that we previously found to occur in Ifnar1−/− mice at day 3 post-IAV (9), suggesting that IFNAR1 alone is able to control bacterial burden more than IFNAR2 alone at day 3 post-IAV. This evidence concerns the gene IFNAR1 and bathing suit ichthyosis.