TP53 and urinary bladder cancer: BKPyV LT-Ag acts as an oncogene in the rare cases where it is permanently integrated into the host genome of bladder cancers (12); by contrast, in the BKPyV-driven cismutagenesis hypothesis, transient LT-Ag sequestration of p53 and inhibition of its transcription factor activity (22) may create an environment that supports carcinogenesis by allowing normal cells to survive the acquisition of the high mutational burdens associated with bladder tumors.