The excessive release of NF-kB promotes NAFLD through multiple mechanisms (53): a) the activation of liver fibrosis in HSCs; b) the initiation of the inflammatory response in KCs; c) the releasing of inflammatory key cytokines (TNF-α, IL6); d) anti-apoptotic functions and the involvement in hepatocarcinogenesis; e) the inflammatory response during LPS stimulation; f) the promotion of IR (54). This evidence concerns the gene TBCE and metabolic dysfunction-associated steatotic liver disease.