We surmise that the BRAF K601E and TERT C250T mutations worked in synergy in the pathogenesis of our patient’s FTC: this tumor’s tendency to have more aggressive phenotypic characteristics may be due not only to the presence of the TERT promoter mutation, but also to its association with the BRAF K601E mutation. The gene discussed is BRAF; the disease is thyroid cancer, nonmedullary, 2.