Various studies have also provided evidence showing that opposing EC proliferative and migratory responses could present together in different pathologies and mechanistic contexts.2–4 The reader also suggested upregulation of Bmpr2, caveolin (Cav) 1/2, and secreted protein acidic and cysteine rich (Sparc) in PAH as markers of EC proliferation. This evidence concerns the gene SPARC and pulmonary arterial hypertension.