In the present study, our aim was to investigate the effects of GC excess on atherosclerosis development in the APOE*3-Leiden.CETP (E3L.CETP) mouse, a well-established model for human-like lipoprotein metabolism that is prone to develop atherosclerosis upon feeding a cholesterol-containing Western-type diet [19] and is responsive to the hypolipidemic drugs used in the clinic similar to humans [20]–[23] The latter is in sheer contrast to other mouse models for hyperlipidemia and atherosclerosis including apoE-knockout and LDL receptor-knockout mice. Here, LDLR is linked to atherosclerosis.