These loci have previously associated with either low-density lipoprotein cholesterol (LDLR, PCSK9, SORT1, LPA, APOE)17 or triglycerides (APOA5, TRIB1),17 both of which have been causally implicated in AAA development.31 The AAA risk allele for rs7255 near the lipid droplet-associated hydrogenase (LDAH) gene was associated with a decreased risk of hypercholesterolemia, suggesting that a mechanism other than increased serum cholesterol likely links the locus to aneurysmal degeneration. This evidence concerns the gene APOE and triple-A syndrome.