These molecules have been utilized to explore the potential of selective targeting of BRD4 in airway inflammation, based on reports of a critical role for BRD4 in NF-κB-mediated epithelial–mesenchymal transition in an in vitro model of airway epithelial cell culture and in in vivo murine models of pulmonary fibrosis and TLR3-mediated acute airway inflammation [27]. Here, NFKB1 is linked to inflammatory response.