Pulmonary arterial hypertension (PAH) remains deadly despite some available treatment options.1 Diagnosis and therapeutic intervention tend to occur relatively late, particularly because symptoms are nonspecific and become evident when right ventricular (RV) dysfunction is already advanced. This, along with the fact that there are now groups of patients who are recognized as higher risk of developing the disease (ie, family members of inheritable PAH, patients with scleroderma or AIDS), makes the need for biomarkers pressing. Unfortunately, biomarkers with strong screening and prognostic value are lacking. Of the known circulating biomarkers, brain natriuretic peptide and troponin T are the most accepted,1 but both are derived from the right ventricle and, therefore, may only be relevant during RV failure, a relatively late stage of the disease. Moreover, both may also be released by the left ventricle, thereby lacking RV specificity, and are not involved in the pathogenesis of the PAH vascular remodeling. Thus, biomarkers that are relevant to disease pathogenesis and measurable at earlier stages and with some specificity for the pulmonary circulation are needed.