Conversely, CFTR knockout ferrets and CF pigs (comprising CFTR−/−, CFTRF508/F508del, and CFTR-/F508del) demonstrate a severe lung phenotype at birth as concerning mucus plugging in the small and large airways [43–46], indicating that the lack of CFTR expression and/or function is fundamental for lung disease initiation and progression in these larger animal models, mimicking human disease. The gene discussed is CFTR; the disease is cystic fibrosis.