This A>G transition results in an alteration of the extracellular domain of TLR-4, that causes hyporesponsiveness to LPS, reduced epithelial TLR-4 density and exaggerated inflammatory cytokine response.27 A recent study has reported an association of TLR-4 gene polymorphisms with gastroduodenal diseases such as gastric atrophy and hypochlorhydria.28,29TLR-4 substitution was associated with noncardia gastric cancer.30,31. Here, TLR4 is linked to chronic atrophic gastritis.