Akt stimulates aerobic glycolysis in cancer cells, supporting continued growth and survival, mediates bioenergetic stability in epithelial cells (68), and stimulates hepatic SREBP1c and lipogenesis through mTORC1-dependent and independent pathways (69), suggesting that Akt might be involved in regulation of lipid synthesis and accumulation in PAH PAVSMC. This evidence concerns the gene AKT1 and pulmonary arterial hypertension.