Recently, Chen et al. reported that inhibition of HDAC3 and Nuclear Factor Erythroid-Derived 2-Related Factor-2 (Nrf2) mitigates pulmonary fibrosis [128], and Zheng et al. suggested that HDAC3 accelerates pulmonary fibrosis by promoting EMT and inflammation through the Notch1 or STAT1 signaling pathway [72]. The gene discussed is STAT1; the disease is pulmonary fibrosis.