These authors showed that endothelial-cell-expressed TRAF6 induces the expression of proinflammatory mediators that enhance the adhesion and recruitment of macrophages to the endothelium, whereas in myeloid cells the opposite occurs, with TRAF6 deficiency favoring the development of atherosclerosis by inhibiting the expression of IL-10 [27]. This evidence concerns the gene TRAF6 and atherosclerosis.