Due to a lack of studies about the use of Class IIA HDAC-inhibitors in preclinical models of lung fibrosis, published studies about the function, contribution and therapeutic correction of increased HDAC4 and -7 activity in fibrotic lung fibroblasts are yet based on single-gene silencing experiments and on the use of pan-HDAC inhibitors, as mentioned above. The gene discussed is HDAC4; the disease is pulmonary fibrosis.