Thyroid cancer is characterized by several genetic alterations along these two pathways, including rearrangements of the RET (rearranged during transfection; RET/PTC) tyrosine receptor kinase, activating point mutations in the BRAF serine/threonine kinase, in the RAS proto-oncogenes, in the catalytic subunit of the phosphatidyl-inositol 3-Kinase (PI3KCA), or inactivating mutations in the tumor suppressors phosphatase and tensin homolog (PTEN) and TP53 (Table 1). The gene discussed is BRAF; the disease is thyroid gland carcinoma.