Previous evidence has shown that Hdac3 could participate in the regulation of the remodeling and expansion of distant alveolar vesicles into primitive lung alveologenesis through inhibition of miR-17-92 expression (Wang et al. 2016), suggesting that Hdac3 may exert a regulatory role in the abnormal angiogenesis and alveolarization of BPD through inhibiting the expression of miR-17-92 cluster. The gene discussed is HDAC3; the disease is bronchopulmonary dysplasia.