Multiple cellular and extracellular matrix mechanisms contribute to vascular stiffness, including elastin fragmentation, collagen deposition, advanced glycation endproduct (AGE)-mediated collagen and elastin cross-linking, impaired VSMC function and calcification, endothelial dysfunction, inflammation and oxidative stress, among others (Chirinos et al., 2019). The gene discussed is ELN; the disease is endothelial dysfunction.