During vascular inflammation and atherosclerosis in other cell types, such as ECs and macrophages, NF‐κB acts predominantly as a direct transcriptional activator via interaction with major coactivator proteins such as CREB‐binding protein (CBP), p300, steroid receptor‐coactivator‐1 (SRC‐1), and p300/CBP‐associated factor (PCAF).2–3,9 This apparent unique tissue‐specific transcriptional repression by NF‐κB in SMCs in response to vascular injury warrants further investigation to elucidate the detailed molecular mechanisms. The gene discussed is NFKB1; the disease is atherosclerosis.