Several studies had shown that the activation of LXR could inhibit the development of atherosclerosis in mice, induce ATP-binding cassette transporter A1 (ABCA1) and apolipoprotein E gene expression, and increase cholesterol efflux, which lead to a decreased cholesterol burden in the arterial wall, as well as enhanced high-density lipoprotein (HDL) levels [63]. Here, APOE is linked to atherosclerosis.