The loss of function of low-density lipoprotein receptor (LDLR) and Apolipoprotein E (ApoE) has been implicated in the progression of atherosclerosis, the primary culprit for cardiovascular diseases (Mahley, 1988; Hasler-Rapacz et al., 1998; Sehayek et al., 2000; Rader et al., 2003). This evidence concerns the gene LDLR and atherosclerosis.