Gastric MALT lymphomas are clinically and histologically quite distinct from comparable low-grade B-cell lymphomas of lymph nodes. Their histology suggests that immunological mechanisms might be operative in their growth. Given that there is normally no lymphoid tissue in gastric mucosa and that Helicobacter pylori (H. pylori), the only common bacterial antigen in the stomach, results in the accumulation of gastric MALT, the possibility that this organism is implicated in the pathogenesis of gastric lymphoma has been extensively investigated. It appears that most, but not necessarily all, gastric MALT lymphomas arise in MALT acquired in response to H. pylori infection and develop by stepwise accumulation of genetic abnormalities. Early molecular events in the evolution of gastric MALT lymphoma from 'acquired' MALT include trisomy 3, t(11;18)(q21;q21), genetic damage leading to genetic instability, as indicated by the so-called replication error repair (RER) phenotype, and both p53 and c-myc mutations. At this stage in their development, the growth of the lymphomas is driven by contact between the neoplastic B cells and H. pylori specific intra-tumoral T cells. Eradication of H. pylori causes the tumour to enter a latent phase resulting in clinical regression. Later events, such as t(1;14)(p22;q32), appear to be linked to a capacity for autonomous growth, loss of sensitivity to H. pylori and dissemination of the lymphoma beyond the stomach and gastric lymph nodes. Cloning of the breakpoint in t(1;14) has allowed the identification of a new tumour suppresser gene, bc110. High grade transformation of MALT lymphoma has been associated with p53 inactivation, deletions of p16 and t(8;14).