The results suggest a biphasic response to transforming effects of excess PTTG in vivo: Abundant PTTG is apparently sufficient to trigger an initial proliferative burst leading to hyperplasia and tumor initiation, however, inability of these pituitary tumors to undergo persistent further growth, is likely due to proliferation-restraining pathways activated by PTTG overexpression. The gene discussed is PTTG1; the disease is pituitary tumor.