The underlying mechanism might be as follows: firstly, LRP6 is critical in LDL receptor-mediated LDL uptake, which is significant in atherosclerosis; secondly, LRP6 plays an important role in metabolic regulation, including lipid homeostasis and glucose metabolism, thus it is associated with atherosclerosis; lastly, mutant LRP6 could trigger atherosclerosis by activating platelet-derived growth factor (PDGF)-dependent vascular smooth muscle cell differentiation (31, 45). The gene discussed is LDLR; the disease is atherosclerosis.