Firstly, clusterin is only expressed in damaged arteries in the early stages of atherosclerosis, where it may be acting to increase fat and lipid transport, and not in healthy arteries (Ishikawa et al., 1998); secondly, clusterin and APOE form HDL particles in blood plasma together with APOA-I and paraoxonase (Baralla et al., 2015), promoting their transport and processing in the liver (Rizzi et al., 2009); thirdly, clusterin removes cholesterol from macrophage-foam cells, which are a key cell type in atherosclerotic lesions (Gelissen et al., 1998). This evidence concerns the gene CLU and atherosclerosis.