In mice on both LDLR KO and APOE KO background, the depletion of macrophage SR-B1 promotes atherosclerosis via a mechanism independent of its function as a hepatic HDL receptor [104, 105]. In atherosclerotic lesions, macrophages of SR-B1 KO mice are proinflammatory and susceptible to apoptosis [106]. Here, APOE is linked to atherosclerosis.