Dysregulated, highly abundant mutant p53 proteins have the potential to exert an active role in tumor cells, not only via DBD-mediated coaggregation but also via their promiscuous interaction modules in the disordered N- and C-terminal regions, and this may be one of the contributing factors why mutant p53 tumors have a poorer prognosis than wild-type tumors in certain cancers [54, 55]. This evidence concerns the gene TP53 and neoplasm.