TP53 is a gene that encodes for the p53 tumor suppressor protein. P53 protein structure comprises five main regions: the transactivation domain, proline-rich domain, DNA binding domain, tetramerization domain, and a regulatory domain. Domains of the p53 protein are subjected to post-translational modifications and this allows p53 stabilization, oligomerization, and transactivation. Sensor proteins such as ATM, ATR, Chk1, Chk2, HIPK2, DNA-PK, and p14ARF are responsible for initial signal transduction upon cellular stress resulting in p53 post-translational modifications that lead to its activation. P53 has been shown to become activated and integrate many cellular stresses including DNA damage, oncogene activation, hypoxia, replication/translation stress as well as cellular metabolic changes. Somatic mutations in p53 are found across a variety of cancer types mainly in colorectal, head & neck, esophageal, female genital organs (cervical, ovarian, uterine, vaginal & vulvar), lung and pancreas. Compared to other tumor suppressors, p53 is unique as mutations can influence its function into different outcomes: loss-of-function (LOF), dominant-negative (DN), and gain-of-function (GOF).