CDKN1B and lung adenoma: Reverse genetic experiments in mouse models, however, suggest a different scenario: (i) Cdkn1b−/− and Cdkn1b± mice developed intestinal and lung adenomas at higher frequency than wild type mice, yet with similar latency and penetrance (15); (ii) tumors from Cdkn1b± mice did not show mutations of the second Cdkn1b allele; (iii) the CDKN1B protein was still expressed at about 50% of the levels of wild type animals.