In a study, researchers examined the expression of IL-35 during early atherosclerosis and found that IL-35 blocks lysophosphatidylcholine-induced mitochondrial reactive oxygen species, which are required for the induction of site-specific histone 3 lysine 14 acetylation, increased binding of proinflammatory transcription factor activator protein-1 in the promoter of intercellular adhesion molecule-1, and induction of intercellular adhesion molecule-1 transcription in human aortic endothelial cells. Here, ICAM1 is linked to atherosclerosis.