As such, PTTG increases the excretion of bFGF [11], which itself can increase ovarian cancer invasion [35]; therefore, PTTG itself may not directly induce tumorigenesis but acts indirectly on tissues expressing a higher level of bFGF, such as the ovary, fallopian tube, and cervix [36-38] to increase angiogenesis and stimulate expression of other activator genes, such as Ets-1 and urokinase-type plasminogen activator to promote tumor progression. The gene discussed is PLAU; the disease is neoplasm.