Accumulating evidence supports the notion that defective phagocytic clearance of dying cells, or defective “efferocytosis,” is causally linked to the progression of advanced atherosclerosis. In advanced atherosclerotic lesions, defective efferocytosis leads to post‐apoptotic necrosis, expansion of plaque necrotic cores, and susceptibility to atherothrombosis. Both macrophages and DC‐like efferocytes are juxtaposed near expanding necrotic cores, where they engage apoptotic cells. In this Viewpoint, we discuss how reduced efferocytosis by macrophages and CD11c^HI DC‐like cells may combine to reduce overall plaque stability and therefore promote susceptibility to acute atherothrombosis.