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. This evidence concerns the gene KRAS and lung neoplasm.