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 SREBF1 and cancer.