Since, Nrf2 expression is central to limiting oxidative stress and inflammation, the reduced expression of Nrf2 in CF airway epithelium (Chen et al., 2008), and now also demonstrated in pulmonary endothelial cells with dysfunctional CFTR, strongly indicate Nrf2 may be a therapeutic target to limit oxidative stress and airway inflammation by increasing its expression and activation in CF. This evidence concerns the gene NFE2L2 and cystic fibrosis.