BRAF and melanoma: BRAF, a member of the RAF kinase family of serine/threonine protein kinases, is mutated in 40–50 % of melanomas and results most frequently from a valine (V) to glutamic acid (E) substitution at residue 600 (BRAFV600E), rendering mutant BRAF protein which no longer requires dimerization for its activity, and is highly predictive of therapeutic response to the specific BRAF inhibitors, vemurafenib and dabrafenib.