Together, these data demonstrate that miR-34a released from injured hepatocytes can mediate the deleterious impact to surrounding hepatocytes and HSCs, activating HSCs in a paracrine manner and inducing expression of fibrogenic mediators, i.e., α-SMA, TGFβ2, and COL1A1, to sustain the development of liver fibrosis. Here, TGFB2 is linked to Hepatic fibrosis.