Asian countries, and is the second greatest cause of cancer deaths in the world [1,2]. A number of studies have established that Helicobacter pylori infection is a feasible risk factor for gastric cancer through the development of gastric atrophy or subsequent precancerous lesions [3,4]. Severe gastric atrophy and corpuspredominant gastritis, as well as intestinal metaplasia, are generally recognized as predominant predispositions to gastric cancer [5]. Host proinfl ammatory genetic factors, in combination with bacterial virulence factors such as CagA, have been shown to determine the severity of gastric damage and the subsequent clinical outcome of H. pylori infection [6,7].Toll-like receptors (TLRs) are type-I transmembrane proteins with extracellular leucine-rich repeat (LRR) motifs and an intracellular Toll/interleukin-1 receptor (TIR) domain [8]. Toll, the founding member of the TLR family, was initially implicated in the establishment of dorsal-ventral patterning in the early development of the Drosophila embryo. Mammalian TLRs have essential roles in the direct recognition of infectious agents, leading to the activation of both innate and adaptive immune responses via nuclear factor-kappa B (NF-κB) signaling pathways. Ten different human TLRs have been identifi ed [9]. Each TLR recognizes specifi c pathogen-associated molecular patterns (PAMPs), including the recognition of lipoproteins, lipoteichoic acid, and zymosan by TLR2; double-stranded for del/del, and 1.14 (95% CI: 0.89-1.45) for ins/del + del/del, relative to the ins/ins genotype compared with gastric atrophy controls; none of these fi ndings were statistically signifi cant. The TLR2 -196 to 174del polymorphism was not signifi cantly associated with either H. pylori seropositivity or gastric atrophy. Conclusion. Our study did not reproduce the association between gastric cancer risk and the TLR2 -196 to -174del polymorphism in Japanese. Further examinations with suffi cient numbers of study subjects are required to verify our fi ndings.