Han et al. demonstrated that SMAD1 deficiency in either endothelial or smooth muscle cells can predispose mice to pulmonary hypertension due to an impaired BMP4 signaling pathway, suggesting that the BMP downstream mediator (i.e., SMAD1) is also crucial for the BMPR2 signal and the prevention of pulmonary artery hypertension [30]. The gene discussed is BMPR2; the disease is pulmonary hypertension.