In this study, we found that overexpression of miR‐30a suppressed the expression of α‐SMA, TIMP‐1, and Collagen I and caused a growth arrest in HSCs (Fig. 2B–D), suggesting that miR‐30a might negatively regulate liver fibrosis by targeting the process of matrix synthesis through inhibiting the activation of HSCs and reducing the number of HSCs via suppressing cell proliferation. This evidence concerns the gene ACTA1 and Hepatic fibrosis.