In summary, our study identifies a prominent role of IRF1 in the development, progression and instability of atherosclerotic lesions, and provides a mechanism explaining the link between subclinical endotoxemia and atherosclerosis, which is partly attributable to the acceleration of foam cell formation induced by nuclear translocation of IRF1 and activation of genes implicated in cholesterol metabolism. This evidence concerns the gene IRF1 and serum lipopolysaccharide activity.