In PAH, excessive proliferation and apoptosis resistance of PASMCs are driven by overproduction of growth factors such as platelet-derived growth factor (PDGF) and TGF-β, which activate pro-survival and pro-proliferative signaling pathways, including mechanistic target of rapamycin (mTOR) and Akt [2,7,9,11,13,14,15,16]. This evidence concerns the gene MTOR and pulmonary arterial hypertension.