To confirm the presence of functional EP2 receptors in our PAH cells, we used butaprost, a selective EP2 receptor agonist, which has little to no activity at the human IP receptor (Ki ~ 100 μM) or any other prostanoid receptor [24] and fails to elicit an anti-proliferative response in EP2 receptor null-mice [20], or as in this study, to significantly elevate cAMP after treatment with EP2 siRNAs. This evidence concerns the gene PTGER2 and pulmonary arterial hypertension.