In APS, aPL-mediated vascular inflammation, oxidative stress and activation of monocytes, neutrophils and the complement system results in endothelial cell proliferation, fibrous intimal hyperplasia, VSMC dysregulation and a concurrent atherogenic process via oxidized LDL and β2GPI complexes [4, 43], which, in concert with traditional CVRF-mediated endothelial dysfunction, might lead to vascular stiffening. Here, APOH is linked to endothelial dysfunction.