Meanwhile, the HDAC inhibitor suberoylanilide hydroxamic acid induces the apoptosis of primary myofibroblasts, decreases bleomycin (BLM)- stimulated murine model lung fibrosis, and improves lung function by modifying the susceptibility of myofibroblasts to apoptosis (Sanders et al., 2014). Here, HDAC9 is linked to pulmonary fibrosis.