The exposure of HSaVEC to PA-BSA stimulated the production of pro-angiogenic molecules—hepatocyte growth factor, platelet-derived growth factor, angiogenin, trefoil factor 3, insulin-like growth factor binding protein-2, angiopoietin-2, and growth differentiation factor 15—and promoted the release of soluble endothelial cell receptors endoglin/CD105, PECAM1/CD31, VCAM1/CD106, and basigin/CD147, together suggesting a development of endothelial dysfunction (Figure 11). The gene discussed is VCAM1; the disease is endothelial dysfunction.