Together, an excessive mononuclear cells activation, such as MΦ, and an increase of soluble vascular endothelial growth factor (VEGF) receptor-1 (sFlt-1), which reduce the bioavailability of the pro-angiogenic VEGF and placental growth factor (PGF), impair normal angiogenesis (Azimi-Nezhad, 2014; Chau et al., 2017) and trigger functional placental insufficiency, and ultimately, FGR (Conroy et al., 2011). This evidence concerns the gene VEGFA and placental insufficiency.