showed that in humans, DNA synthesis is primarily an early lesion event that slowly halts and gets replaced by apoptosis as lesions advance.30 Our BrdU pulse‐labeling proliferation data supports this concept and reinforces our use of Apoe−/− mice on a chow diet in analyzing the dynamics of macrophage proliferation, as opposed to other, more‐accelerated diet‐induced models of atherosclerosis. The gene discussed is APOE; the disease is atherosclerosis.