While TGF-β, IL-6, fatty acids, or angiotensin II produced in NASH may be involved in stimulating CCN2 production among the various hepatic cell types [45], our results show that the exposure of hepatocytes to free fatty acid results in their production of pro-fibrogenic EVs that induce transcription of CCN2 and other fibrosis-related molecules (Col1A1, αSMA) in HSC. This evidence concerns the gene ACTA1 and metabolic dysfunction-associated steatohepatitis.