As in other cancer types in which BRAF was shown to be a prominent oncogene, it was soon clear in preclinical studies that BRAF V600E signaling through MEK-ERK was essential for driving thyroid oncogenesis; inhibiting such signaling in genetically engineered mouse models expressing BRAF V600E blocked tumor transformation and paved the way for the development of specific inhibitors as a new strategy for the treatment of thyroid cancer. The gene discussed is BRAF; the disease is neoplasm.