Despite the fact that the mechanisms through which obesity increases the risk of preeclampsia have not been fully explained, some data strongly suggest that those involved concern: activated macrophages and uterine natural killer cells, which perform a crucial role in placental development; the activation of peripheral T helper cells inducing the production of cytokines, including TNF-α, IL-6 and IL-17; as well as the anti-angiogenic agent sFlt-1, and B cells that produce angiotensin type 1 receptor agonistic autoantibodies (AT1-aa). This evidence concerns the gene IL17A and obesity due to melanocortin 4 receptor deficiency.