In patients with pulmonary diseases characterized by chronic bacterial infections, such as cystic fibrosis, airway neutrophils inhibit T-cell function via two pathways — by depletion of arginine following degranulation and activation of Arginase-1 (Arg1), and by activation of the programmed death ligand-1 (PD-L1)/programmed death-1 (PD-1) axis, resulting in reduced proliferation and impaired effector functions6–15. This evidence concerns the gene ARG1 and cystic fibrosis.