When compared with healthy fetuses, lower levels of ECFCs, with lower capacities in vitro and in vivo, have been isolated from fetuses with IUGR, probably because of unbalanced antiangiogenic factors (e.g., thrombospondin-1) and proangiogenic factors (e.g., MMP-2 and SDF-1) [136,171]. This evidence concerns the gene CXCL12 and fetal growth restriction.