For example, the expression of PPARγ was increased in late onset preeclampsia, but not early onset preeclampsia, compared to normal pregnancy [40]; the activation of PPARγ by its agonist rosiglitazone can probably relieve the preeclampsia by reducing uterine perfusion pressure and benefiting placental vasculature [41,42]; PPARγ plays an important role in controlling endothelial function and blood pressure homeostasis, which is crucial for pathological preeclampsia [43]. This evidence concerns the gene PPARG and preeclampsia.