To dissect the mechanisms by which SMC-specific NEMO deficiency reduced macrophage accumulation in the lesions of ApoE−/− mice and thus atherosclerosis severity we analysed the expression of adhesion molecules, chemokines, cytokines and metalloproteases in aortic arches isolated from NEMOSMCiKO/ApoE−/− mice or their littermate ApoE−/− controls after 10 weeks of HFD feeding. The gene discussed is IKBKG; the disease is atherosclerosis.