GSDMD is the primary substrate of caspase-11, and the N-terminal GSDMD cleavage fragment generated (GSDMD-NT) leads to the formation of pores (protein channels) in the plasma membrane and secretion of caspase-1 produced IL-1β and other caspase-1 dependent secretomes and caspase-11-dependent secretomes (139, 146) into the extracellular space to promote liver inflammation (NASH), and subsequently increased hepatic pyroptosis and promotes NAFLD. Here, IL1B is linked to metabolic dysfunction-associated steatotic liver disease.