There is insufficient information to rationalize the connection between GCN2 and lung vascular pathophysiology, but an interesting hypothesis is that mutations that compromise GCN2 stress response function may expose pulmonary environment to more oxidative stress, which may predispose both mouse pulmonary hypertensive models and human subjects to pulmonary hypertension (Eyries et al., 2014). This evidence concerns the gene EIF2AK4 and pulmonary arterial hypertension.