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Zinc status, inflammation, and genetic determinants are prominent mechanisms in the pathogenesis of atherosclerosis (AT) and its compliances (cardiovascular diseases). In this review, we report the possible impact of zinc on AT development as well as the role played by a significant genetic determinant involved in inflammation, such as interleukin-6 (IL-6). Genetic polymorphism of IL-6 may affect a different inflammatory response as well as zinc turnover, predisposing to AT. Indeed, zinc deficiency is suggested as a risk factor for AT with advancing aging. The increment of dysfunctional proteins involved in zinc homeostasis, i.e. metallothioneins (MT), caused by persistent inflammation and oxidative stress may further contribute to zinc deficiency and consequently to the development of AT. A zinc supplementation may be useful to achieve healthy aging and, as such, to prevent AT, but it is necessary to consider the individual genetic background (especially when referred to IL-6 and MT polymorphisms) for the success of zinc intervention. Therefore, a zinc genomic approach may offer a reasonable hope for understanding the impact of zinc on molecular processes that maintain health and prevent the development of AT.