Several weaknesses are associated with this study. The SSc-PAH population was older than the population with SSc but no PAH (mean 61.0 ± 11.0 years vs 52.0 ± 9.7 years, P = .0029) and the IPAH cohort (51.0 ± 13.6 years, P = .0013). Therefore, age could have influenced our findings. We note, however, that this discrepancy mirrors the age difference found between SSc populations with and without PAH and may be a difficult confounder to avoid. Another weakness was the time difference between RHC and measurement of GDF-15 levels. However, ECHO results were much closer to the blood draw, and estimated RVSP correlated significantly with GDF-15 levels in plasma. Few patients diagnosed with SSc without PAH underwent RHC to definitively confirm the absence of PAH. However, we carefully excluded PAH in this cohort by setting stringent requirements for ECHO, Dlco, and physical examination. Furthermore, we followed this patient population prospectively for a mean of 2.8 years, confirming the lack of clinical evidence of PAH. SSc-PAH is a progressive disease and we feel confident that our SSc without PAH cohort were, in fact, true PAH-negative at the time of the blood draw. Almost all patients were on multiple PAH treatments (Table 2). Although we cannot exclude treatment as a possible cause of differences in plasma GDF-15, no individual treatment correlated with GDF-15 levels, including prostacyclins (P = .31). GDF-15 measurements were taken at one specific point in time. Future studies could examine GDF-15 levels over multiple time points, or by assessing changes with therapy. We did not exclude subjects with interstitial lung disease in this study, which could have been a potential confounder. Finally, Mathai et al25 recently reported that levels of NT-proBNP predicted survival in subjects with SSc-PAH, but not in those with IPAH. We did not find the same predictive strength for NT-proBNP in our study, possibly because of the larger number of subjects in the Mathai study.