TP53 and cancer: Because, 1) Vpr blocks proliferation of cancerous cells by induction of cell cycle G2 arrest [1], [2], and this arresting effect is independent of the classic DNA checkpoints [3], [4]; 2) Vpr induces apoptosis through multiple pathways that do not depend upon host cellular responses [5], [6]; and 3) Vpr selectively kills fast growing cells in a p53-independent manner [7], [8], suggesting Vpr-induced cell death may offer more selectively power in killing cancerous cells than normal cells and this cytotoxic property should be effective in many of the cancers, in which p53 gene is mutated.