Moreover, XN exhibited various inhibitory activities toward issues associated with hepatic steatosis, e.g., downregulation of expression of chemokine monocyte chemotactic protein 1 (MCP-1) and the cytokine (CXCL1) causing (non-alcoholic) steatohepatitis (an advanced stage of fatty liver disease) and hampering hepatic infiltration progress of inflammatory cells (validated through CD3-immunohistochemical analysis). This evidence concerns the gene CCL2 and fatty liver disease.