The increased expression of adhesion molecules such as ICAM-1, VCAM-1 and E-selectin, the enhancement of pro-inflammatory cytokines (TNF-α, IL-1, IL-6, IFN-γ), and the upregulation of oxidative stress processes are the starting point of this condition [23]; moreover, also the increase of leptin and resistin (proatherogenic hormones) and the decrease of adiponectin (antiatherogenic hormones) may alter endothelial homeostasis in RA patients [22]. Here, TNF is linked to rheumatoid arthritis.