TP53 and cancer: Conversely, it has also beenshown that p53 activation and subsequent MDM2 upregulation both enhancereplication fork progression and increase replication fork processivity (Klusmann et al., 2016).Although these findings appear conflicting, it is tempting to speculate thatdisruption of the p53/MDM2 axis in human cancers, either byTP53 mutation or MDM2 overexpression, may interfere withorigin firing and replication fork stability.