Considering the common pathobiological mechanisms of pulmonary hypertension and pulmonary fibrosis, including dysregulated angiogenesis, endothelial dysfunction, and endothelial to mesenchymal transition [36, 37], inhibition of G6PD activity might be a common mechanism of impact of DHEA in pulmonary hypertension and fibrosis [38]. The gene discussed is G6PD; the disease is endothelial dysfunction.