Along with HSC activation, subsequent upregulation of both sterol regulatory element-binding protein 2 (SREBP2) and miR-33a signaling through the suppression of PPARγ signaling, as well as disruption of the SREBP2-mediated cholesterol-feedback system in HSCs, which was characterized by a high SREBP cleavage-activating protein (Scap)-to- insulin-induced gene (Insig) ratio and exaggerated by the down-regulation of Insig-1 through the suppression of PPARc signaling, led to further FC accumulation and enhancing liver fibrosis in a positive feedforward loop. Here, SREBF2 is linked to Hepatic fibrosis.