The authors have hypothesized that iodine-deficiency (I-def) or in some cases iodine-excess (I-excess) is associated with the development of gastric cancer. They report a short review of their own work and general literature on this subject in three fields: (1) epidemiology, where geographical and temporal correlations between territories with I-def (or I-excess) endemic goitre and high GC-death rate are reported; (2) immunology, where the possible correlations between I-def, immune-deficiency and GC are reported; and (3) thyroid gland and stomach correlations, both being embryologically derived from primitive gut and able to concentrate iodine. This ability is impaired by nitrates, thiocyanate, salt and by I-excess, which in fact can cause goitre. In our study I-def goitrous people have shown more atrophic gastritis than normal subjects. These data enable us to hypothesize that I-def or I-excess might constitute a new risk factor for gastric cancer, both by regulating gastric trophism and by antagonizing the action of those I-inhibitors (such as nitrates, thiocyanate and salt) previously studied as risk factors for gastric cancer.