We conclude that the Lrp1Y63F mutation not only promotes the accumulation of ApoB48 remnants, as also seen in the hepatic Lrp1 knockout (Rohlmann et al., 1998; Rohlmann et al., 1996), but also causes decreases in HDL and ApoA1, which could independently increase atherosclerosis reminiscent of the increased risk of premature atherosclerosis in individuals with Tangier’s disease (Tall and Wang, 2000). This evidence concerns the gene APOA1 and atherosclerosis.