As reported, macrophages that infiltrated into plaques often play a crucial role in the development of atherosclerosis.[29] Intraplaque proinflammatory microenvironment can switch the macrophages in the plaques to M1 macrophages, which play a major role in proinflammatory factors’ secretion.[30] Modulation of macrophage phenotypes is a novel strategy for the treatment of atherosclerosis.[31] Since 3‐HB reduced intraplaque macrophage infiltration of apoE−/− mice (Figure 2), we set out to determine whether 3‐HB can reduce the proportion of intraplaque M1 macrophages. This evidence concerns the gene APOE and atherosclerosis.