Our data suggest that preferential engagement of the IRF7 or NF-κB pathway may determine the effect of TLR9 stimulation in macrophages on plaque formation.36,37 Koulis et al have shown that TLR9 deletion promoted atherosclerosis, and that treatment with the TLR9 ligand CpG ODN 1668 reduced atherosclerosis.36 On the other hand, Krogmann et al demonstrated that treatment of atherosclerotic Apoe−/− mice with CpG ODN 1826 enhanced atherosclerosis.37 Our data support a proatherogenic role of the TLR9-IRF7 pathway. Here, TLR9 is linked to atherosclerosis.