BMPR2 and pulmonary arterial hypertension: Increasing BMPR2 shuttling to the membrane using the chaperone 4-phenylbutyric acid (4PBA) [65] led to a mild improvement in BMPR2 downstream signaling in patient fibroblasts that contained a specific inactivating mutation C118W, which served as a proof of concept for the applicability of this method in patients and an important step towards precision medicine in PAH [66].