Oncogenic conversion of cell signaling pathways involving mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase/protein kinase B (AKT) has been identified in the pathogenesis of thyroid cancer.1BRAF (MAP3K), RAS (small GTP-binding protein), and RET (receptor tyrosine kinase) are drivers of the MAPK signaling cascade that have been of particular interest over the past 13 years.5,6 Incidence of BRAF mutations varies according to histologic subtype and geographic location, with rates ranging from 28% to 83%.3,4,7,8. The gene discussed is AKT1; the disease is thyroid gland carcinoma.