These inhibitors encompass: (a) hydroxamic acids such as TSA (a naturally occurring compound), SAHA, panobinostat (LBH589), and parcinostat (SB939); (b) cyclic peptides, notably romidepsin (FK228); (c) synthetic compounds such as 4-phenylbutyrate sodium, benzamide MS-275 (entinostat), and CG-745; and (d) subtype-specific HDAC inhibitors, including the short-chain fatty acid VPA, RGFP966, NCC170, tubacin, and tubastatin A. Table 1 encapsulates the overarching therapeutic impacts of diverse HDAC inhibitors on preclinical models pertaining to lung fibrosis/IPF. Here, HDAC9 is linked to idiopathic pulmonary fibrosis.