HIF1α has been shown to be stabilized under normoxic conditions in experimental and human PAH, and activation of HIF1α can induce glutamine reliance.36, , –39 We found that BMPR2 mutant PMVECs grown in culture exhibited significant normoxic stabilization of HIF1α at the protein level compared to WT (Fig. 5a and 5b), and that this was demonstrable for two different PAH-associated BMPR2 mutation types. The gene discussed is HIF1A; the disease is pulmonary arterial hypertension.