TLR4-mediated inflammation was previously reported to participate in the pathogenesis of atherosclerosis.9, 12 In the present study, we found that HF diet significantly accelerated the formation of atherosclerotic plaque in ApoE−/− mice but not in ApoE/TLR4−/− mice, although significant intimal hyperplasia was presented in ApoE/TLR4−/− mice (Figure 2a). The gene discussed is TLR4; the disease is atherosclerosis.