Conclusion: We conclude that IL-6 -174, low producer genotypes, may have an important role in gastric carcinogenesis and the polymorphism study of this molecule could be a good marker for gastric carcinoma susceptibility when high grade dysplasia is seen in biopsies. Objective: In Helicobacter pylori gastritis, constant antigenic stimulation triggers a sustained B-cell proliferation. Errors made during this continuous DNA replication are corrected by the DNA mismatch repair mechanism. Failure of this mechanism has been described in HNPCC and results in a replication error phenotype. Inherent to their instability during replication, microsatellites are the best markers of this replication error phenotype. We aimed to evaluate the role of defects in the DNA mismatch repair mechanism and microsatellite instability (MSI) in gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Method: We examined 10 microsatellite loci (BAT25, BAT26, D5S346, D17S250, D2S123, TGFB, BAT40, D18S58, D17S787 and D18S69) for instability in 28 patients with MALT lymphomas. In addition, these tumors were also immunostained for MLH1, MSH2 and MSH6, as well as screened for the presence of t(11;198)(q21;q21) by real time polymerase chain reaction (RT-PCR). Results: We found MSI in 5/28 (18 %) lymphomas, with one tumor displaying high levels of instability. MSI occurred in both t(11;18)(q21;q21)-positive and -negative tumors. Conclusion: Our data suggest that a MMR-defect may be involved in the development of gastric MALT lymphomas, and mutations in the MSH6 MMR gene or hypermethylation of the MSH6 promoter might be associated with MSIdriven gastric lymphomas.