Cellular activation of the proinflammatory transcription factor NF‐κB causes nuclear translocation of p65‐p50 dimers and thus enhances expression of genes whose protein products (such as ICAM‐1 and VCAM‐1) mediate leukocyte recruitment under inflammation and consequently contribute toward vascular inflammation and atherosclerosis 48, 49. This evidence concerns the gene NFKB1 and atherosclerosis.