Bidirectional crosstalk between gut microbiota and bile acids could impair the intestinal epithelial function, increasing the translocation of gut-derived endotoxins such as LPS to the blood and lymphatics to activate hepatic TLR-4/NF-κB signaling and promote NAFLD or NASH [108,109]. Here, TLR4 is linked to metabolic dysfunction-associated steatohepatitis.