Wang Zhi-min et al excluded a link between XP and exon mutations of the LDLR gene or familial hypercholesterolemia and demonstrated that high-density lipoprotein level might be implicated in XP pathogenesis.[16] Similarly, Li Yong-rong et al found no significant differences in single nucleotide polymorphisms of macrophage scavenger receptor 1 (MSR1), a gene related to atherosclerosis, between XP patients and healthy controls. The gene discussed is LDLR; the disease is familial hypercholesterolemia.