LDLR and atherosclerosis: The specific deletion of Tet2 in myeloid cells, but not other lineages, in mice further suggests that the altered response of Tet+/− or Tet−/− macrophages to high levels of LDL (i.e., a high-cholesterol diet) is sufficient to increase aortic lesions and to induce atherosclerosis in Ldlr knock-out animals [32].