Furthermore, the SLC7A5 inhibitor 2-aminobicyclo(2,2,1)-heptane-2-carboxylic acid (BCH) was reported to inhibit mTOR signaling (90) and hence might be able to attenuate glutaminolysis-induced fibrosis resulting from αKG-mediated mTOR activation and proline hydroxylation in PAH (35). This evidence concerns the gene MTOR and pulmonary arterial hypertension.