TP53 and cancer: Since some oncogenic alterations such as myelocytomatosis (MYC) deregulation, TP53 or retinoblastoma protein (RB) deletion are known to underly mitotic defects in cancer and prime cells for even further disruption of mitotic processes [34–37], interfering with the mitotic localization of AURKB might amplify these mitotic vulnerabilities better than inhibiting AURKB catalytic activity [38].