BRAF and melanoma: Current data indicate that BRAF non-V600 mutations generally exhibit a poor overall response to BRAF inhibitor monotherapy.12 However, combined BRAF/MEK inhibition could be considered for these mutations.13 The clinical significance of specific BRAF mutations is further exemplified by the findings showing that BRAF fusions are more sensitive to sorafenib, which is a kinase inhibitor more selective for CRAF than BRAF when compared to specific BRAF-specific inhibitors such as vemurafinib14,15 (sorafenib induces apoptosis in melanoma cells with non-V600E mutations15).