The study investigates the mechanism of macrophage accumulation in atherosclerotic lesions, challenging the prevailing notion that monocyte infiltration is the primary driver. Using murine models and advanced imaging techniques, the authors demonstrate that macrophages in established atherosclerotic lesions undergo rapid proliferation, primarily driven by local proliferation rather than monocyte recruitment. This rapid turnover is orchestrated by scavenger receptor class A (SR-A), which plays a crucial role in macrophage proliferation. The findings suggest that targeting macrophage proliferation could be a therapeutic strategy for cardiovascular diseases.The study investigates the mechanism of macrophage accumulation in atherosclerotic lesions, challenging the prevailing notion that monocyte infiltration is the primary driver. Using murine models and advanced imaging techniques, the authors demonstrate that macrophages in established atherosclerotic lesions undergo rapid proliferation, primarily driven by local proliferation rather than monocyte recruitment. This rapid turnover is orchestrated by scavenger receptor class A (SR-A), which plays a crucial role in macrophage proliferation. The findings suggest that targeting macrophage proliferation could be a therapeutic strategy for cardiovascular diseases.