The similarities between atherosclerosis in humans and mice deficient either in apoE (Plump et al., 1992; Zhang et al., 1992; Nakashima et al., 1994; Breslow, 1996) or the LDL receptor (Ishibashi et al., 1993) suggest that molecular mechanisms underlying regression in these mouse models could be relevant to the reduction in plaque burden in the human population (Williams et al., 2007, 2008; Feig et al., 2009). Here, LDLR is linked to atherosclerosis.