Although Perp has roles both in intercellular adhesion and p53-dependent apoptosis, the effects of Perp deficiency on tumor latency and tumor-free survival in this mouse cancer model likely result from altered desmosome-mediated cell-cell adhesion, because the tumors are null for p53. Collectively, our results therefore indicate that Perp can display tumor-suppressor activities in more than one type of epithelial cancer and that Perp deficiency can promote tumor development in the context of different tumor-promoting stimuli. The gene discussed is PERP; the disease is neoplasm.