Both 3-MA, a chemical inhibitor of autophagy, and transfection with siRNAs targeting Atg3 and Atg7 inhibited autophagy in HSCs and in the livers of CCL4- or TAA-treated mice and reduced lipid metabolism and energy production, which then inhibited ECM production and liver fibrosis 13. Here, CCL4 is linked to Hepatic fibrosis.