Despite recent progress, pulmonary arterial hypertension (PAH) remains without a cure. The impact of the approved drugs on PAH is small and, with the exception of some parenteral therapies, they have little or uncertain effects on haemodynamics, right ventricular (RV) function and survival. There are two main reasons for this. First, the complexity of this vascular remodelling disease is high and its pathology includes fundamental mechanisms from several other diseases and syndromes, including neoplasia (the anti-apoptotic and pro-proliferative remodelling within the vessel wall), degenerative diseases (the early loss of endothelial cells and microvessels) and inflammation 1. In addition, a reversal of vascular remodelling will mean little unless it is accompanied by a reversal of RV failure, which at this point remains clinically unpredictable. Secondly, whatever therapy is developed, it needs to be directed against the unique features of PAH and should be selective for the pulmonary circulation, sparing the often normal systemic vessels 1. This second factor is perhaps the most challenging. One of the common features of all existing therapies for PAH is that they were originally developed for systemic vascular diseases and it was only after they either failed or determined to be non-profitable, that they were tested on PAH. Surprisingly, there are several quite promising therapies for PAH which remain untested in humans. One of the main reasons is the lack of continuity and the poor efficiency in translational research 1. Typically, one team might perform cellular work, another small animal work, another large animal work and another phase 1 trials, before phase 2 and 3 trials are planned. This usually takes many years. In the current issue of the European Respiratory Journal ( ERJ ) 2 and a very recent issue of the ERJ 3, the same team from Giessen (Germany), in collaboration with …