For example, the Gram-negative bacteria structural element LPS was suggested to be elevated in portal vein in ALD and cirrhosis.326 Mechanistically, Seki et al. described that, upon LPS binding, TLR4 upregulates chemokine secretion and downregulates TGF-β pseudoreceptor Bambi to enhance TGF-β signaling pathway.327 The study also suggested that the effect of LPS is mediated by MyD88-NF-κB-dependent pathway, as MyD88-deficient mice had decreased hepatic fibrosis. The gene discussed is MYD88; the disease is Cirrhosis.