The research conducted by Li et al. reported a new defensive function for LH1 against dissecting AAA; the absence of LH1 determines an upregulation of thrombospondin-1 (encoded by Thbs1) expression, thus promoting the proinflammatory process, increasing matrix metalloproteinase (MMP) activity, and severe apoptosis of vascular smooth muscle cells in the abdominal aorta, the final result being the dissecting AAA formation. Here, PLOD1 is linked to triple-A syndrome.