For independent validation of the role of CFTR as a modifier of early airway disease in βENaC-Tg mice, we next crossed βENaC-Tg mice with gut-corrected CF mice [14] and compared survival, early mucus obstruction and airway epithelial necrosis in neonatal single-transgenic βENaC-Tg mice and double-mutant βENaC-Tg/CF mice (Fig. 5). The gene discussed is CFTR; the disease is cystic fibrosis.