In addition, using the choline-deficient L-amino-defined (CDAA)-diet-induced NASH model, TLR2 deficiency improved hepatic inflammation and injury by reducing Kupffer cell inflammasome activation and pro-inflammatory cytokine production, suggesting a KC-dependent inflammatory pathway mediated by TLR2 [96]. This evidence concerns the gene TLR2 and metabolic dysfunction-associated steatohepatitis.