IL-1β has emerged as a key driver in the exacerbation of hepatic inflammation, steatosis, injury, and fibrosis, and promotes significant production of TNF-α and monocyte chemoattractant protein-1 (MCP-1), collectively contributing to the development of NAFLD/NASH.463,467–469 In the mouse model, hepatic production of MCP-1, TNF-α, and IL-1β is significantly reduced in GSDMD−/− mice. Here, TNF is linked to metabolic dysfunction-associated steatohepatitis.