The latency period for tumors to develop in these transgenic mice would also suggest that mutant p53(273H) combine with other age-related genetic or epigenetic alterations, such as mutation at codon 12 or 13 of K-ras gene and inactivation of p16 by methylation of its promoter region, to promote lung tumor formation and progression in the p53(273H) transgenics. Here, CDKN2A is linked to lung neoplasm.