TLR4 and metabolic dysfunction-associated steatohepatitis: One mechanism for the development of NASH involves LPS, a TLR4 agonist derived from enterobacterial flora; LPS reaches the liver in large amounts and increases the secretion of proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, by stimulating Kupffer cells [10, 13, 31].