The results of our in vitro experiments on the effect of aspirin on atherosclerosis showed elevated protein levels of PPARδ, AMPK, PGC-1α, and eNOS in the aspirin-treated group compared to the levels in the high-fatty acid and high-cholesterol group without aspirin; however, these increases were reversed by treatment with the PPARδ antagonist GSK0660 (Figure 1(a), A-1–A-4). This evidence concerns the gene PPARGC1A and atherosclerosis.