Hypothesis shows that the proinflammatory cytokines especially interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) contribute to the occurrence and development of NASH, and consequently lead to liver cirrhosis and hepatocellular carcinoma.3,4 Therefore, down-regulating the expression of the proinflammatory cytokines might be a practical therapeutic strategy for NASH. The gene discussed is IL6; the disease is metabolic dysfunction-associated steatohepatitis.