Ruffin et al. (2018) showed that the inflammatory response of primary differentiated CF airway cells to bacterial toxins is reduced by ivacaftor/lumacaftor, dependent on the rescue of CFTR activity. However, this does not explain oxidative stress and enhanced pro-inflammatory signaling in CF epithelial cells under basal conditions reported by us previously (Stolarczyk and Scholte, 2018; Stolarczyk et al., 2018), which may contribute to the development of early CF lung disease. The gene discussed is CFTR; the disease is cystic fibrosis.