Considering that in vitro and ex vivo models of Pseudomonas aeruginosa (PA) infection show that mucus downregulates the basal levels of bacterial virulence genes [55,56], we can speculate that alteration of mucin homeostasis and the mucin network in bronchiectasis contributes to mucociliary impairment and increased susceptibility to infection. The gene discussed is MUC5AC; the disease is infection.