Three are the functional consequences of these single amino acid substitutions: i) abrogation of tumor suppressor activities largely due to the inability to recognize wild-type p53 (wtp53) consensus sequences on DNA; ii) inhibition of the tumor suppressor function of the remaining wtp53 allele because of a dominant negative effect; iii) acquisition of new oncogenic properties, commonly described as mutant p53 (mutp53) gain of function, which can actively contribute to various aspects of tumor progression [1]. This evidence concerns the gene TP53 and neoplasm.