Metabolic insults, such as increased SFAs, proinflammatory adipokines, hyperglycemia, etc., promote K+ efflux, mitochondrial dysfunction and ROS production, lysosomal disruption, etc., leading to NLRP3 inflammasome activation and caspase-1-mediated IL-1β and IL-18 secretion and pyroptosis, which in turn mediate a systemic cascading inflammatory response. The gene discussed is IL1B; the disease is Hyperglycemia.