Contrary to an earlier study showing that the activation of BAT exacerbates atherosclerosis in mice lacking the low-density lipoprotein (LDL)-receptor or apolipoprotein E (ApoE) (6), we have shown that BAT activation not only corrects hypertriglyceridemia (7) but also reduces plasma cholesterol levels and atherosclerosis in transgenic mice expressing both a loss-of-function variant of human apolipoprotein E (APOE*3-Leiden; E3L) and the human cholesteryl ester transfer protein (E3L.CETP mice) (8). The gene discussed is APOE; the disease is atherosclerosis.