I obtained Ph.D in Physiology in Chinese University of Hong Kong in 2008. During postdoctoral fellowship, in the Brigham and Women's Hospital and Harvard Medical School in Boston, I have specialized in studying Transforming growth factor (TGF)β signaling in cardiopulmonary diseases. Currently, I am an Instructor of Medicine in the Harvard Medical School. Dysregulated TGFβ signaling is an important driver of pulmonary hypertension and vascular remodeling. However, previous approaches were not clinically translatable due to systemic and cardiac toxicity associated with broad inhibition of TGFβ , Activin, and Growth and differentiation factor (GDF) signaling. It was postulated that cardiac toxicity might be attributable to the undesirable impact of disrupting TGFβ2 signaling, causing the degeneration of cardiac valve tissues which depend on this signaling axis for constitutive endothelial-mesenchymal transition. To test this concept, I used a soluble TGFβ type II receptor (TGFBRII-Fc), which could block TGFβ1 and TGFβ3 signaling on smooth muscle phenotype, while leaving TGFβ2 and BMP ligand signaling intact. I have demonstrated that TGFBRII-Fc exerted a beneficial impact on pulmonary hypertension, vascular remodeling, and right ventricular function in 3 animal models, but without cardiac valve toxicity. These results were recently published in the American Journal of Respiratory and Critical Care Medicine. This paper was recommended as “exceptional” in F1000 Prime. Our work was also selected as the Best Basic Science Abstract for the 2016 Pulmonary Hypertension Association International Conference and Scientific Sessions, where I was honored to present one of two selected abstracts. This work was also recognized with a Research Excellence Award from the Brigham Research Institute in the Brigham and Women's Hospital. In recognition of the clinical potential of this approach, the patent application for this technology was recently licensed by Acceleron Pharma, Inc., and pre-clinical toxicology studies are now ongoing.