The exact mechanism behind the activation of pulmonary bile acid synthesis is unknown, but it may be a consequence of endothelial dysfunction, which then act as steroid hormones and serve as substrates for nuclear membrane receptors and/or g-protein copied receptor signaling gene transcriptions for major enzymes in bile acid synthesis (such as CYP7A1 and CYP8B1) and other key proteins in cell cycle regulation—processes that have been shown in cancer metastases (45, 46). The gene discussed is CYP7A1; the disease is endothelial dysfunction.