In response to cellular stress, the p53 protein experiences post-translational modifications, such as phosphorylation and acetylation [7,8], which allow for its accumulation and translocation into the nucleus, where it activates target genes involved in cell cycle arrest, apoptosis, senescence, anti-angiogenesis and autophagy, thereby suppressing malignant tumor transformation and preserving genomic integrity [9,10]. The gene discussed is TP53; the disease is cancer.