This epistatic relationship between Brca2 and Palb2 lends further support to the notion that the two gene products function as a complex in tumor suppression, whereas the delayed tumor formation in B1P2p53 and B1B2p53 mice suggests that BRCA1 and the PALB2/BRCA2 complex not only share similar fundamental tumor-suppressive activity but also possess mutually independent functions that influence the progression of the tumorigenic process, possibly by impacting cell fitness. Here, PALB2 is linked to neoplasm.