In fact, the aforementioned studies focused on the effect of exogenous FN-EDA on HSCs; however, our data, including some unpublished data, suggested that HSCs were the dominant source of FN-EDA during hepatic fibrosis and that interfering with FN-EDA expression in vitro decreased the expression of α-SMA and VEGFA but not collagen, indicating that HSC derived FN-EDA, rather than exogenous FN-EDA, is important to maintain HSC activation. This evidence concerns the gene ACTA1 and Hepatic fibrosis.