Without altering circulating total cholesterol, triglycerides or HDL, or lipid profile (Supplementary Table 1 and Supplementary Fig. 4b), the provision of exogenous 27HC increased early plaque formation and early atherosclerosis progression in apoE−/− mice expressing endothelial ERα, but not in apoE-/- lacking endothelial ERα (Fig.  2c–f). The gene discussed is APOE; the disease is atherosclerosis.