Other cytokines overexpressed in SLE, such as TNF-α, IL-17, and IL-6, participate in the initiation and perpetuation of the atherosclerotic process by stimulating the activation of macrophages, inducing the secretion of matrix metalloproteinases, upregulating the expression of adhesion molecules on the ECs, increasing the concentration of chemotactic messengers, and affecting the proliferation of smooth muscle cells [15, 55–59]. This evidence concerns the gene IL6 and systemic lupus erythematosus.