Excessive activation of the MAPK signaling pathway, which increases the risk of PTC development and progression, may be caused by mutations in the B-Raf proto-oncogene, serine/threonine kinase gene, BRAF. BRAF mutations are the most common gene mutations in PTC; in particular, previous studies have suggested that more than 50% of thyroid cancers have the BRAFV600E mutation [3], which is associated with lymph node metastasis, extrathyroidal invasion, and advanced disease stage [4–6]. This evidence concerns the gene BRAF and metastatic malignant neoplasm in the lymph nodes.