Not only has it been shown that CF airway macrophages are hyperinflammatory, a phenotype that perhaps is independent of defective CFTR chloride channel function [61], but it is also highly possible that an overly exuberant innate immune/inflammatory response and influx of proteases may maladaptively drive bronchiectatic changes by both leading to “unchecked” tissue damage and diminishing the restorative capacity of the lung. Here, CFTR is linked to cystic fibrosis.