ACTA1 and Hepatic fibrosis: The CRISPR-dCas9 system was used to activate the expression of endogenous MIAT (Fig. 7C), and the up-regulated MIAT significantly increased the hepatic fibrosis markers α-SMA, collagen I, and MMP9 of LX-2 (Fig. 7C, D) and promoted cell proliferation (Fig. 7E).