Possible candidates include: (a) human soluble VEGFR2 (160 kDa) – present in significant quantities in healthy human plasma (7–8 ng/mL) [140] and upregulated in acute myeloid leukemia [39]; (b) soluble NRP1 (90 kDa) – a VEGF165-specific antagonist, with documented renal expression in humans [141], [142]; and (c) cellular fibronectin (∼500 kDa) – with VEGF-affinity sites on its heparin-binding domain [124], [143] and normally present in extracellular matrix but can end up in elevated amounts in plasma upon endothelial dysfunction or vascular injury, such as in pre-eclampsia [144]. The gene discussed is FN1; the disease is endothelial dysfunction.