To potentially intervene in this process, Pinderski et al. sought to more closely examine the pathogenesis of a previously observed therapeutic role for IL-10 in inhibiting the development and progression of atherosclerotic lesions.39–42 They first developed a transgenic mouse model wherein IL-10 overexpression is localized only to activated T lymphocytes, then successfully engrafted transgenic or wild-type bone marrow into low-density lipoprotein receptor-deficient mice—a phenotype that induces constitutive hyperlipidemia—fed an atherogenic diet. This evidence concerns the gene VLDLR and hyperlipidemia.