KDM6B and Hepatic fibrosis: We should acknowledge that this study has limitations and only provided, for the first time, in vitro evidence to support JMJD3 as key negative regulator against HSCs activation, HSCs-targeted Jmjd3 transgene in vivo investigation in mouse models with adeno-associated viral vector, which is enabled to host large gene sequences like Jmjd372, is highly warranted to further elucidate the function of JMJD3 in liver fibrosis and its possible translational application for epigenetic gene therapy.