Gene lesions associated with well-differentiated forms, in particular BRAF and RAS mutations, are also frequently found in PDTC and ATC in association with additional alterations (such as PI3K, PTEN, TP53 and TERT promoter mutations [5]), supporting the model of tumor progression from pre-existing PTC or FTC driven by sequential accumulation of multiple genetic abnormalities. The gene discussed is BRAF; the disease is neoplasm.