Lung fibrosis was largely attributable to prolonged NF-κB signaling in mice lacking YAP/TAZ in ATII cells, as IκBα (NFκB inhibitor α) was discovered to be a direct target of YAP/TAZ and their associated transcription factor, TEAD (TEA domain family) [285]. Here, NFKB1 is linked to pulmonary fibrosis.