Recent studies have shown evidence of important roles for chemokines in the pathogenesis of MASLD, and Ccl2 and Ccl5 are recognized as important mediators in liver damage and inflammatory tissues, as they are associated with macrophages.39 Previous studies have shown evidence that LPS-stimulated macrophages contribute to the inflammatory response by activating members of the NF-κB transcription factor family.40 Here, we speculated that LPS is a metabolite that can inhibit macrophage activity and inhibit the NF-kB signaling pathway due to IPA and IAA treatment. The gene discussed is CCL2; the disease is metabolic dysfunction-associated steatotic liver disease.