Cl− enters in cotransport with Na+, and can leave the cell along an electrochemical gradient on the apical side through CFTR, resulting in Cl−-driven fluid secretion and subsequently alveolar liquid accumulation as seen in pulmonary edema and ARDS (Weidenfeld and Kuebler, 2017), and TNF alpha upregulates NKCC1 mRNA and protein levels. The gene discussed is CFTR; the disease is pulmonary edema.