In 43% of cases, at least half of the mutations detected in the initial tumor were not present in the recurrent tumor, including driver mutations in TP53, ATRX, SMARCA4, and BRAF, indicating that recurrent tumors may be seeded by cells of the initial tumor at an early stage of development, and each tumor accumulates its own set of genomic alterations [15]. Here, BRAF is linked to neoplasm.