Endothelial dysfunction is the first step in atherogenesis and its development in RA is associated with multiple factors: systemic inflammation, proinflammatory cytokines (TNF-α, IL-6, IL-1, IFN-γ, and IL-17), oxidative stress, disbalance of certain hormones (leptin, resistin, and adiponectin), increased expression of adhesion molecules, altered endothelial progenitor cell function, immune dysregulation, genetic predisposition, as well as traditional factors such as diabetes mellitus, arterial hypertension, and high body mass index [25]. Here, TNF is linked to rheumatoid arthritis.