* Silencing NR2F2 in human endothelial cells causes inflammation, increased cell migration, resistance to apoptosis, and changes related to vascular damage, while also elevating DKK1 levels, which is associated with pulmonary arterial hypertension.
* Therapeutic strategies that either activate NR2F2 or block DKK1 might offer potential treatments for chronic vascular diseases linked to endothelial cell dysfunction.