Another group already demonstrated that human HSCs express CCL5 when challenged with TNF-alpha, IL-1beta, or CD40L in vitro13, but our work suggests for the first time that HSCs express Ccl5 in early NASH to directly induce steatosis and upregulation of pro-inflammatory factors in hepatocytes. This evidence concerns the gene CCL5 and metabolic dysfunction-associated steatohepatitis.