Different mechanisms involving the role of aPL in the process of AT have been described, and these include overexpression of tissue factor, annexin I and II, cytokines and other mediators of endothelial dysfunction [39]–[41]; oxidative perturbations and mitochondrial dysfunction [42]; and cross-reactivity with oxidized low-density lipoproteins, accelerating their influx into macrophage and AT development [43]. This evidence concerns the gene F3 and endothelial dysfunction.