These mechanisms of this context-dependent tumorigenesis versus tumor suppression may not be unique to PLK1, and may be a result of CIN regulatory feedback loops that aid cellular response to insult [195], but nonetheless, these conflicting results show the importance of the complex role of CIN and PLK1 and using a less conventional approaches to indirect targeting PLK1 overexpression in cancer. The gene discussed is PLK1; the disease is neoplasm.