Previous study have shown that apolipoprotein C1 (ApoC1) overexpression in ApoE−/− mice can exacerbate atherosclerosis by promoting severe hypertriglyceridemia, increasing very low density lipoprotein (VLDL) synthesis and reducing lipid residue clearance by lipoprotein lipase, which may be related to the pathogenesis of AAA. Here, LPL is linked to triple-A syndrome.