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ing to Hp-related CVD risk; Hp-I is associated with increased tumor necrosis factor alpha (TNF-a), a circulating cytokine able to exert its effects at a distance. TNF-a and interleukin (IL)26 (TNF-a is the main trigger for the production of IL-6 by a variety of cells) play important roles in the regulation of synthesis of other acute phase proteins, which are established risk factors for atherosclerosis, such as the mentioned fibrinogen and factor VIII; and circulating lipid peroxides, also associated with cardiovascular risk, are raised in Hp-positive patients. Therefore, Hp eradication might display a positive effect on Hprelated NAFLD and CVD development/progression by inhibiting various prothrombotic and proinflammatory agents partly in some Hp-positive ethnic subpopulations. Because there is a lack of literature showing any demonstrable evidence to support the aforementioned hypothesis, large-scale studies are warranted to elucidate our hypothesis.