This concept (Figure 7) was based on the evidence that (1) GEO data GSE15197 analysis and the previous study on the proteomic analysis [21] suggested the differential expression of TUFM in PAH and normal control; (2) silencing TUFM prevented the rat from development of PAH induced by MCT; (3) Si-TUFM inhibited mitophagy and improved apoptosis of PASMCs under hypoxia condition, and (4) the activity of AMPK and its downstream molecule mTOR were regulated by TUFM in PASMCs. The gene discussed is MTOR; the disease is pulmonary arterial hypertension.