A number of clinical trials are evaluating the efficacy of inhibitors of the RAS/RAF/MEK/ERK signaling pathways as well as small molecule inhibitors of BRAFV600E in these tumor types (NCT01748149).19 The specific BRAF alteration is correlated to response to treatment; KIAA1549–BRAF fusions are RAF-independent and BRAFV600E mutations are responsive to autophagy and small molecule inhibitors.11,12,14 Two of the tumors evaluated in this study were found to harbor BRAFV600E and would have the potential for BRAF-targeted inhibition. The gene discussed is BRAF; the disease is neoplasm.