These included RNAs in pathways relevant to PAH; for example, SMAD5 (mothers against decapentaplegic homolog-5), encoding a downstream mediator of signaling of BMPR2 (3), was reduced in patients with PAH (Figure 2C), consistent with documented reduced BMPR2 signaling in this condition, and the transient receptor potential cation channel, TRPC1 (Figure 2D), also associated with the development of PH (18), was also reduced in patients. This evidence concerns the gene SMAD5 and pulmonary arterial hypertension.