The suppression of key signaling molecules involved in the canonical signaling pathways of pyroptosis, (e.g., NLRP3, caspase-1, IL-1β, and GSDMD), was able to attenuate pathological changes such as hepatic steatosis, inflammation, and early fibrogenesis in animal models of NAFLD/NASH. This evidence concerns the gene IL1B and metabolic dysfunction-associated steatotic liver disease.