This dysbiosis may be an important factor in causing NASH, in mouse models and human, through different mechanisms like deregulating energy homeostasis, modulation of choline and bile acid metabolism, and generation of bacteria-derived toxins, such as lipopolysaccharide (LPS), and increased hepatic TNF-a expression (through TLR4 and TLR9-dependent profibrotic pathways) in hepatic Kupffer cells (178–181). The gene discussed is TLR4; the disease is metabolic dysfunction-associated steatohepatitis.