Macrophages from patients with cystic fibrosis, who have dysfunctional chloride currents due to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene, are characterised by persistent pro-inflammatory activation and defective phagocytosis, facilitating chronic infection [50,51]. The gene discussed is CFTR; the disease is cystic fibrosis.