The development of a pro-inflammatory state in CF epithelial cells and lymphocytes is also due to the reduced production and nuclear localization of peroxisome proliferator-activated receptors (PPARs), transcription factors that normally counteract the action of NF-κB, which is activated by the hyperproduction of reactive oxygen species (ROS) [33,34,35,36]. Here, NFKB1 is linked to cystic fibrosis.