Several factors can promote tumor development including: (1) p53 mutations that activate the formation of the Smads2/3 and p63 complex that suppresses the action of p63 allowing TGF-ß to promote EMT; (2) loss of Smad4 function secondary to genetic alterations; (3) overexpression of Six1 (pro-metastatic regulator); (4) oncogenic activation of the Ras-RAF-MAPK pathway; (5) hypomethylation of the PDGFβ gene; and (6) DAB2 epigenetic downregulation [178]. This evidence concerns the gene TP53 and neoplasm.