In the present study, we not only demonstrated that the suppression of NLRP3 inflammasome as an intracellular inflammatory machinery during NASH is an underlying mechanism responsible for the anti-inflammatory action of FTZ but also interestingly confirmed that FTZ inhibits lipid deposition in liver cells by the blockade of NLRP3 inflammasome-mediated HMGB1 production. The gene discussed is HMGB1; the disease is metabolic dysfunction-associated steatohepatitis.