By using transgenic FGF9-OE mice, which over-express FGF9 in the conducting airway epithelium, Hiller et al. (2022) [69] found that, in contrast with their control littermates, FGF9-OE mice exhibit increased morbidity, delayed viral clearance, and significantly more histopathology changes related to severe inflammation after infection with the influenza WSN strain. The gene discussed is FGF9; the disease is influenza.