Using Tet2−/− mice and transferring their bone marrow to that of Ldlr−/− mice, which are prone to atherosclerosis due to knockout of the LDL receptor, Jaiswal et al.16 showed that mice that had the Tet2-deficient bone marrow had significantly larger atherosclerotic plaques in the aorta despite having a similar fasting serum lipid profile as control mice. The gene discussed is LDLR; the disease is atherosclerosis.