On the other hand, recent advances revealed a relatively high prevalence of genetic alterations in the RET-Ras-BRAF signaling cascade and other unique chromosomal rearrangements in thyroid cancer and demonstrated that most PDTC or ATC derive from pre-existing well-differentiated thyroid cancer through additional genetic alterations, including β-catenin nuclear accumulation and p53 inactivation [7]. This evidence concerns the gene TP53 and thyroid cancer.