Studies demonstrate that TP53 mutation not only results in loss of cell cycle checkpoint function, diminished DNA damage repair capacity, and promotion of tumor initiation and progression, thereby correlating strongly with an aggressive phenotype, chemotherapy resistance, and poor prognosis in bladder cancer, but also promotes the formation of an inflammatory microenvironment via activation of the NF-κB signaling pathway. This evidence concerns the gene TP53 and urinary bladder cancer.