Of the seven patients in our cohort whose tumors acquired hemizygous CDKN2A deletions, none had concurrent BRAFV600E mutations at diagnosis or progression, but four had BRAF fusions which were conserved over time; further research is thus needed to determine whether hemizygous CDKN2A loss and BRAF fusions may act synergistically in facilitating tumor growth. The gene discussed is CDKN2A; the disease is neoplasm.