During the last few years, increasing evidences illustrate the role of NLRP3 in NASH (83–85), elevated hepatic expression of Nlrp3, Asc, and Casp1 associates with liver inflammation in dietary and nutrient deficiency fatty liver diseases (84, 86–88), and NLRP3 activation is critical for progression of NASH evidenced by genetic knockout mice and NLRP3 pharmacological inhibitor (12, 89, 90). This evidence concerns the gene CASP1 and metabolic dysfunction-associated steatohepatitis.