In their in vitro study on human aortic endothelial cells, Wang et al. suggested that the favourable effects of apremilast on atherosclerosis may be explained by (i) the reduction in the expression of lectin-like oxidized-LDL receptor-1, (ii) the inhibition of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-8, and (iii) decreasing monocyte adhesion to endothelial cells, which is a key factor in atherosclerosis pathogenesis [27]. This evidence concerns the gene IL6 and atherosclerosis.