P53 aggregation leads to loss of tumor suppressor function, FUS aggregation promotes neurodegenerative diseases and tumor metastasis, and YAP/TAZ condensates drive cellular stemness—these processes are all associated with imbalance of endogenous physiological regulation.[64, 77] The low sequence complexity of the EBNA1 PrLD allows evasion of host immune surveillance in the EBV genome while maintaining stability of viral genetic material through a prion‐like phenotype, a viral adaptive strategy not possessed by cellular proteins. This evidence concerns the gene TP53 and neurodegenerative disease.