Furthermore, we identified that silencing NR4A2 did not alter the expression or secretion of sFlt-1 or PGF, key factors central to the pathogenesis of preeclampsia, suggesting that placental NR4A2 is not involved in driving the release of anti-angiogenic factors from the dysfunctional placenta, a key process in the pathogenesis of preeclampsia. The gene discussed is NR4A2; the disease is preeclampsia.