Because both global and hematopoietic deletions in the murine CAD risk orthologous locus led to increased atherosclerosis, global Chr4Δ70kb/Δ70kbLdlr−/−ApoB100/100 mice showed increased blood leukocyte count, and Chr4Δ70kb/Δ70kb BMDMs showed more pro-inflammatory phenotype in vitro, we decided to investigate if human ANRIL and its murine equivalent (Figure 5A) are expressed in inflammatory cell populations in atherosclerotic plaques, and how their expression levels are in comparison with other vascular cell populations. This evidence concerns the gene CDKN2B-AS1 and coronary artery disorder.