In a rat model of nonalcoholic fatty liver disease (NAFLD) induced by high-fat and high-cholesterol diet, the lipotoxic injury-induced release of miR-192-5p-enriched hepatocyte exosomes played a critical role in M1 macrophage activation; miR-192-5p drove macrophages to polarize towards the proinflammatory M1 phenotype through modulating the Rictor/Akt/FoxO1 signaling pathway, which resulted in hepatic inflammatory response, demonstrating that exosomal miR-192-5p is a key player in the NAFLD-mediated activation of M1 macrophages (51). The gene discussed is AKT1; the disease is metabolic dysfunction-associated steatotic liver disease.