This finding indicates the interrelation between the LPS and the pathogenesis of NASH, and between LPS and the activation of HSCs through binding to TLR4, TLR9 and other TLRs followed by HSC proliferation and collagen production ([86], reviewed in [73,74,84]), as well as between endothelial TLR4 and fibrosis-associated angiogenesis [87] and between TLR4 and angiotensin-II in fibrogenesis of NASH [88]. The gene discussed is AGT; the disease is metabolic dysfunction-associated steatohepatitis.