In contrast with these beneficial effects in hypertriglyceridemia, BA activation of PXR, a well-known transcription regulator in the control of lipid metabolism [50,103], increased levels of total cholesterol, VLDL, and LDL; decreased high-density lipoprotein (HDL) levels; and increased atherosclerosis in ApoE−/− mice [104], while PXR deletion reduced atherosclerosis in ApoE−/− mice [105]. The gene discussed is APOE; the disease is atherosclerosis.