HDAC3 and idiopathic pulmonary fibrosis: The lack of nuclear HDAC3 activity in IPF fibroblasts may have substantial implications for disease development and progression because, in other cellular models, HDAC3 participates in establishing the genetic profile necessary for cell proliferation, migration, apoptosis, autophagy, and senescence; all of these processes are also related to IPF [30,31,32,33].