We recently reported that apart from its CFTR rescuing property, GSNO augmentation by using either GSNO or a GSNOR-inhibitor (N6022) effectively diminished CS-induced inflammatory-oxidative stress and also corrected the autophagy impairment (Bodas et al., 2017), thus targeting the underlying cause of CFTR dysfunction and resulting CF lung disease pathogenesis and progression. The gene discussed is ADH5; the disease is cystic fibrosis.