Moreover, frequent TP53 mutation hotspots, particularly in the DNA-binding domain, such as arginine 175, 248, 249, 273, and 282 (R175, R248, R249, R273, and R282), as well as glycine 245 (G245), disrupt its canonical tumor suppressor functions and contribute to tumorigenesis and progression10–12. This evidence concerns the gene TP53 and neoplasm.