Similar to acute liver failure, inflammatory mediators such as IL-6, TNF-α, TGF-β [35], MCP-1 and RANTES [23, 36] are crucially involved in the pathogenesis of NASH including insulin resistance, steatosis and apoptosis of hepatocytes, immune cell infiltration, and liver fibrosis all of which could be greatly ameliorated by UDCA-LPE accompanied by a downregulation of inflammatory mediators including MCP-1 and TNF-α [14]. The gene discussed is CCL2; the disease is steatosis.