BRAF and cancer: Approximately 40% of patients with ATC have a targetable BRAFV600E mutation.2 BRAFV600E mutation results in constitutive activation of BRAF and the downstream MAPK pathway, a major oncogenic pathway for cancer initiation and progression.7 Treatment of BRAFV600E-mutated ATC with a combination of BRAF and MEK inhibitors has resulted in dramatic response rates that are substantially improved from chemoradiation.8 As such, patients with BRAFV600E-mutated ATC on a BRAF/MEK inhibitor have a median overall survival (OS) of 14.5 months.9,10