The results of animal experiments by Ki et al. suggested that H. pylori endotoxins that transported in the portal vein to the liver, coupled with liver injury by CCl4, might accelerate hepatic fibrosis through increasing TGF-b1-inducing proinflammatory signaling mediated by ERK and NF-kB in HSCs (25). The gene discussed is NFKB1; the disease is Hepatic fibrosis.