IL1B and metabolic dysfunction-associated steatohepatitis: The pathogenesis of MASH involves three interconnected pathological processes: chronic inflammatory response mediated by pro-inflammatory mediators [such as TNF-α (Tumor Necrosis Factor-alpha), IL-6 (Interleukin-6), IL-1β (Interleukin-1 beta), ROS (Reactive Oxygen Species)], programmed hepatocyte death, and fibrosis progression mediated by hepatic stellate cell activation (35).