Several CDK inhibitor knockout models, including p18 and p27, also exhibited pituitary tumors (23, 33), while models of combined CDK inhibitor knockout shortened latency of tumor formation or increased size of pituitary tumors, including knockout of p21/Rb (34), p27/Rb (35), p16/p18 (36), p27/cyclin E (37), p27/p18 (33), p21/p18 (38), and CDK4/p27 (39). The gene discussed is RB1; the disease is neoplasm.