Recently, studies have reported that HDAC3 promotes pulmonary fibrosis; Chen et al. reported that inhibition of HDAC3 and Nuclear Factor Erythroid-Derived 2-Related Factor-2 (Nrf2) mitigates pulmonary fibrosis28, and Zheng et al. suggested that HDAC3 accelerates pulmonary fibrosis by promoting EMT and inflammation through the Notch1 or STAT1 signaling pathway29. The gene discussed is STAT1; the disease is pulmonary fibrosis.