We hypothesize that overexpression of Plscr1 in ciliated epithelial cells would not be able to rescue susceptibility in Ifnlr1-/- mice or cells, as the Plscr1-/-;Ifnlr1-/- mouse model suggests that Plscr1’s Ifn-λr1-independent anti-influenza mechanisms are likely minor compared to its role in upregulating Ifn-λr1. Here, PLSCR1 is linked to influenza.