Hyperglycemia maternal promotes the production of reactive oxygen species (ROS), resulting in oxidative stress, which can contribute to the proinflammatory environment typical of diabetes (Cvitic et al., 2014) and placental hypervascularization, with alterations in vasculogenesis and VEGF-R1 and R2 receptors (Pietro et al., 2010). Here, FLT1 is linked to diabetes mellitus.