We previously determined that absence of CD36 inhibited atherosclerosis lesion development in 12-week Western diet fed apoE degrees mice, and this was due largely to absence of macrophage CD36. It is possible that at later stages of disease this effect would be lost due to the progressive nature of lesion development and involvement of other factors. However, lesion development continues to be characterized by recruitment of macrophages and foam cell formation, thus it is also possible that delay in lipid accumulation as a result of absence of CD36 would continue to retard lesion development. The objective of this study was to determine if absence of CD36 continued to inhibit lesion formation. Background matched apoE degrees and CD36 degrees /apoE degrees mice were fed a Western diet for up to 35 weeks. At 20 and 35 weeks, lesion area was 25 and 35% less, respectively, in CD36 degrees /apoE degrees mice. Most impressive was the difference in gross appearance of the aortas at 35 weeks: apoE degrees aortas were sclerotic and nearly occluded by lesion, whereas aortas from CD36 degrees /apoE degrees mice had smaller lesions that were more punctate. We conclude that absence of CD36 continues to reduce lesion burden even at late stages of disease in the apoE degrees model.