While expression of mutant Kras is by itself sufficient to generate the entire histological spectrum of PanIN lesions, the penetrance of developing invasive cancer, the time to progression to invasive cancer, and the predominant histology of the cancers that arise vary depending on additional genetic alterations, such as mutation of Trp53 or loss of Cdkn2A/Ink4 function, that are engineered simultaneously with Kras. This evidence concerns the gene TP53 and cancer.