While BRAFi/MEKi monotherapies and combinations have shown high ORR and significantly prolonged PFS and OS in V600E and, to a lesser extent, V600K-mutated melanoma [3••–4••, 9••, 33–34], efficacy in non-V600 mutations depends on their role of BRAF as a genetic driver for tumor proliferation and the existence of other concurrent mutations in key cell signaling pathways [22]. The gene discussed is BRAF; the disease is neoplasm.