Indeed, we have demonstrated this case using the K18-driven system in ovarian surface epithelium, wherein lesions disrupting p53 function facilitate progression to metastatic stage IV serous ovarian cancer [28], and in mammary epithelium, where Trp53 and BRCA1 deletion progresses hyperplasia to adenocarcinoma (Van Dyke et al., unpublished). This evidence concerns the gene TP53 and ovarian serous adenocarcinoma.