This endotoxemia stimulates the activation of toll-like receptor 4 (TLR4) [78] and inflammatory signaling cascades including the NF-kB pathway, which results in the production of pro-inflammatory cytokines that promote hepatic inflammation and oxidative stress, which are key components of MASLD pathophysiology [79]. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatotic liver disease.