In line with these findings, peptidyl-prolyl isomerase (Pin1: an important driver of proliferation and inflammation) was found to be increased in the lung tissue of patients with PAH, cultured human pulmonary microvascular ECs, and animal models, with its inhibition being able to reverse pulmonary vascular remodeling by interacting with members of the transforming growth factor β (TGF-β)/bone morphogenetic protein (BMP)-mediated signaling (21). This evidence concerns the gene TGFB1 and pulmonary arterial hypertension.