Approximately 50% of human cancers have mutations in the TP53 gene itself, while the rest of them harbor functionally inactive p53 proteins, because active p53 can trigger cell growth arrest, apoptosis, autophagy, and/or senescence, which are detrimental to cancer cells (Vogelstein et al., 2000; Vousden and Prives, 2009), and impede cell migration, metabolism, and/or angiogenesis. This evidence concerns the gene TP53 and cancer.