CTSS is involved in the pathogenesis of cardiovascular diseases via its effect on extracellular matrix protein degradation, protein transport, and cell signaling.[28] CTSS can be secreted into the extracellular matrix via lysosomes, increasing collagen and elastin degradation, promoting vascular smooth muscle migration, and ultimately causing atherosclerosis.[29] Apoptosis of the medial smooth muscle cells of the arterial wall is an important marker of AAA, with an increase in apoptosis during aneurysm formation. Here, ELN is linked to triple-A syndrome.