Blockade of toll-like receptor 4 on Kupffer cells and other immune cells, preventing activation by LPS (an endotoxin) from the gut. Inhibiting the LPS–TLR4 pathway reduces NF-κB–mediated inflammatory cytokine release and curtails downstream stellate cell activation and fibrogenesis in the liver. The goal is to interrupt gut-derived inflammation, which drives NASH. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatohepatitis.