Of note, sEng (i) displays pro-inflammatory activity via nuclear factor-kappa B (NFκB) and interleukin 6 (IL6) in human endothelial cells [52]; (ii) shows antiangiogenic activity and increased vascular permeability in vitro and in vivo [40,51,53]; (iii) modulates inflammation-associated monocyte adhesion and transmigration [13]; (iv) contributes to endothelial dysfunction, as shown in transgenic animals overexpressing human sEng [54,55]; and (v) regulates vascular development and arteriovenous malformations by modulating angiogenesis [47]. The gene discussed is IL6; the disease is endothelial dysfunction.