This not only conflicts with our observation of Bmpr2 downregulation in PAH,1 but also with the expression plot in their letter and findings in the wider PAH field of reduced BMPR2 signalling,5 EC hyperproliferation in Cav1 and Cav2 knockout mice,6 and unclear contributions of SPARC in proliferation and angiogenesis.7 Furthermore, we do not believe they are as direct or established a marker of proliferation as cell cycle–related genes (e.g. Mki67, Pcna, and Mcm genes). The gene discussed is CAV1; the disease is pulmonary arterial hypertension.