Some experimental studies have shown that gastric ulcers induced by acetic acid have a multifactorial process that begins with the depletion of the mucous content of the stomach wall, associated with excessive production of free radicals in consequence to an increase in the proinflammatory interleukins TNF-α, IL-1β, and IL-6, accompanied by an increase in neutrophil infiltration into the gastric mucosa [21, 35–37]. The gene discussed is TNF; the disease is gastric ulcer.