A short-term treatment with an anti-CTLA-4 antibody led to endothelial activation, accelerated the progression of atherosclerosis by inducing a predominantly T cell-driven inflammation, and resulted in the formation of plaques with larger necrotic cores and less collagen in an in vivo atherosclerosis experimental model based on hypercholesterolemic, low-density lipoprotein receptor (LDL-R) knock-out mice (ldlr−/− mice) (11). This evidence concerns the gene LDLR and atherosclerosis.