Subsequent validation of pracrinostat revealed that it attenuated FMD through the derepression of the antifibrotic gene PGC1A and the suppression of various cytokine and ECM genes in TGF-β-stimulated IPF fibroblasts, which was, in part, attributed to the abrogation of HDAC7-mediated TGF-β signalling [246]. Here, HDAC7 is linked to idiopathic pulmonary fibrosis.