Overexpression of all class I and II HDACs, particularly HDAC2 and HDAC4, significantly contributed to the progression of pulmonary fibrosis by activating the proliferation of lung fibroblasts into apoptosis-resistant myofibroblasts and increasing the expression of ECM protein-coding genes such as α-SMA and collagen type I [34,48]. Here, ACTA1 is linked to pulmonary fibrosis.