A number of studies have demonstrated that EVs contribute to key processes involved in the pathogenesis and progression of NAFLD, including angiogenesis, fibrosis, and inflammation.271–273 The EVs secreted by hepatocytes can promote the expression of proinflammatory cytokines and polarize hepatic macrophages to the M1 phenotype.274–276 Mixed-lineage kinase 3 (MLK3) induces lipid-treated hepatocytes to release EVs containing CXCL10 to recruit macrophages. This evidence concerns the gene MAP3K11 and metabolic dysfunction-associated steatotic liver disease.