Of note, the fibroblasts isolated from IPF patient lungs indicate reduced levels of COX2 or NRF2 even after 6 or more passages [162,258,259], hinting at the involvement of epigenetic repression mechanisms and that HDAC-mediated gene repression of antifibrotic molecules precedes growth-factor-induced profibrotic gene expression in IPF. Here, HDAC9 is linked to idiopathic pulmonary fibrosis.