Experimental data have extended the knowledge of the mere association of gastric mucosa associated lymphoid tissue (MALT) lymphoma and infection with Helicobacter pylori.The acquisition of MALT in the stomach is a direct consequence of the infection; thus MALT in the stomach is formed as an immunological defence system to control local infection caused byH pylori. Lymphomas arising from gastric MALT show several specific features: they arise from the marginal zone of the lymphoid follicle, they consist of centrocyte-like cells, and lymphoepithelial destruction must be present in order to establish the diagnosis of gastric MALT lymphoma.1 ,2 The genetic events that lead to clonal evolution and, finally, malignant transformation also show that MALT lymphomas have specific features not known from nodal lymphomas—for example, the translocation t(11;18). Data concerning other genetic events like rearrangements of oncogenes such as bcl-2 (translocation t(14;18) in follicular lymphoma), c-my (translocation t(8;14) in Burkitt's lymphoma), or bcl-l(translocation t(11;14) in small cell lymphoma/chronic lymphocytic leukaemia) have not been reported to be significantly associated with gastric MALT lymphoma. Furthermore, numerical chromosomal abnormalities—that is, trisomy 3, 7, or 12—have not been reported to be consistently involved in the cases analysed.3-7 In contrast, the translocation t(11;18) has been associated with marginal zone B cell lymphomas. Ott et al reported that up to 40% of low grade MALT lymphomas of different mucosal sites showed the translocation t(11;18)(q2l;q2l).8 The recently identified genes involved in this translocation APJ2 (apoptosis inhibitor gene 2 on chromosome 11) and MLT (MALT lymphoma translocation gene on chromosome 18) have not been fully functionally classified.9 ,10 It has been reported that lymphomas responding to H pylori therapy are t(11;18) negative,11 thus this translocation may be associated with more advanced disease. In keeping with these …