Thyroid cancer initiation and progression occurs through gradual accumulation of various genetic and epigenetic alterations, such as activating mutations of the BRAFV600E, RET/PTC rearrangement, PTEN deficiency, and TP53 mutations, that involve the activation of MAPK and PI3K/AKT signaling pathways 5, 6. This evidence concerns the gene TP53 and thyroid gland carcinoma.