One of the best examples of the latter class is amplification or overexpression of Mdm2, which was observed in a subset of human tumors, some of which retain wild-type p53[33] leading to the conclusion that increased levels of MDM2 directly contribute to human tumor formation by substituting for mutations in p53 gene, which represents an alternative mechanism by which tumor cells escape from the tumor suppressive activities of p53. Here, TP53 is linked to neoplasm.