Surprisingly, initial studies using LDL receptor deficient (LDLR−/−) mice with a macrophage‐specific deletion of IκB kinase 2 (IKK2), showed increased atherosclerosis with more advanced lesions and more necrotic plaques.6 These results highlight the importance of NF‐κB in the gene program promoting the resolution of inflammation. Here, NFKB1 is linked to atherosclerosis.