p53 mutational patterns often bear the etiological fingerprints of carcinogens [9]: For example, p53 mutation hotspots in skin cancer are located at sequences containing contiguous pyrimidines that are the preferential sites for ultraviolet (UV) photodimer formation; p53 mutational hotspots in cigarette smoke (CS)-related lung cancer are located at cytosine methylated -CG- sites that are preferential binding locations for CS carcinogens such as the diol epoxide forms of polycyclic aromatic hydrocarbons (PAHs) and acrolein (Acr) [5, 10–13]. This evidence concerns the gene TP53 and skin neoplasm.