Further, hyperinsulinemia increases the expression of M1 macrophages and modulates the mammalian target of rapamycin complex 1 (mTORC1) pathway, thus inducing an imbalance between pro-inflammatory (increased) and anti-inflammatory (reduced) T-lymphocyte populations [65], overall contributing to heightening both systemic and placental inflammatory states; furthermore, it acts locally at the maternal–fetal interface, reducing the number of decidual natural killer cells (dNKs) and vascular endothelial growth factor (VEGF) production while increasing TNF-α [58]. Here, VEGFA is linked to hyperinsulinism.