TP53 and neoplasm: In addition to the DNA repair related, cell-intrinsic radiosensitivity mechanisms, other possibilities include incomplete TP53 inactivation [34], expression of radiosensitizing E6 isoforms [74], or prolonged G2/M arrest [35]; there are also cell-extrinsic proposed mechanisms involving the tumor microenvironment, such as decreased tumor hypoxia and improved immunoreactivity, which are nicely reviewed elsewhere [39,75,76].