In NASH, the intestinal defense mechanism is disrupted (i.e., leaky gut), and the increased influx of lipopolysaccharide (LPS) derived from intestinal bacteria into the liver results in the excessive production of inflammatory cytokines such as TNF-α via TLR4 signaling in Kupffer cells, which promotes liver fibrosis in NASH [73]. Here, TLR4 is linked to metabolic dysfunction-associated steatohepatitis.