Moreover, circulating Th cells do not produce cytokines “at rest” but need to be activated to start producing cytokines. Gaowa et al2 also analyzed the IL17A-producing T cells, as we did, after in vitro stimulation of isolated circulating T cells, to have a direct quantification of Th17 cells. They found an increase in peripheral Th17 cells and in RORγt messenger RNA levels (a transcription factor that drives the Th17 lineage commitment). Importantly, the Th17/regulatory T-cell subsets ratio was significantly related to the severity and prognosis of CTD-aPAH. Moreover, microarray data confirmed that gene functional groups shared by systemic sclerosis associated-PAH and idiopathic PAH lungs include IL17A signaling.3 Importantly, IL21, which is mainly derived from Th17 cells, plays a critical role in the pathogenesis of experimental PAH in mice,4 and one can expect similar mechanisms in patients with PAH.