New avenues demonstrate the potential role of STAT3 in decreased expression of BMPR2 in PAH.28 As mentioned, BMPR2 and PPARγ are implicated in PAH pathology, and some links seem to exist between these factors.9 Furthermore, in chondrocytes, RAGE can regulate PPARγ expression and activation.29 All these data led us to our hypothesis that RAGE activation by S100A4 triggers STAT3 activation, decreasing BMPR2 and PPARγ in pulmonary smooth‐muscle cells and leading to the proproliferative and apoptosis‐resistant phenotype found in PAH. Here, S100A4 is linked to pulmonary arterial hypertension.