Further mechanistic studies have revealed that ACLY plays a crucial role in the activation of the NLRP3 inflammasome, characterized by the following observations: inhibition of hepatic ACLY leads to an increase in fatty acid oxidation in liver cells, a reduction in fatty acid and sterol synthesis, and a mitigation of hepatic steatosis and ballooning. Here, NLRP3 is linked to Hepatic steatosis.