The main pathogenic mechanisms which are considered to be involved include the occurring hypergastrinemia in cases of atrophic gastritis, as described above, the increase of the intraluminal ammonia products, which can trigger intracellular tumorigenic mechanisms, and finally the promotion of systemic inflammation, through overexpression of proinflammatory cytokines (IL-1, IL-8, TNF-α, etc) and growth factors (EGF, TGF-α, etc) [28]. This evidence concerns the gene EGF and chronic atrophic gastritis.