This is in contrast to many other tumor suppressor genes that undergo deletion through the course of tumor initiation or development, such as PTEN, BRCA1, and Rb. Five arginine residues in the p53 gene are considered mutational “hotspots”; resultant mutant proteins fail to bind to sequence-specific DNA sites and therefore drastically alter the spectrum of transcriptional activity (15). Here, TP53 is linked to neoplasm.