For example, interferon γ (IFN-γ) secretion induced by H. pylori promotes an inflammatory milieu that exacerbates disease severity [29], and this cytokine, along with IL-6 and IL-13, promote EBV proliferation, and higher levels of proinflammatory cytokines, including IL-1β, tumor necrosis factor α (TNF-α) and IL-8, have been reported to promote severe gastritis associated EBV and H. pylori co-infection [10]. The gene discussed is TNF; the disease is coinfection.