Previous studies illustrated that lipid accumulation in hepatocytes induced the production of IL-8, which was a significant discriminator of non-alcoholic steatohepatitis severity due to its association with the advancement of steatosis (16, 21, 22), which may partly explain why the level of IL-8 in our cohort is lower than those from previous western studies. Here, CXCL8 is linked to metabolic dysfunction-associated steatohepatitis.