However, lack of hot-spot BRAF, RAS, or NF1 driver mutations in the triple wild-type subtype accounting for 6–20% of melanomas [2, 3], and variability of phenotype of patient-derived melanoma cell lines representing the same genetic subtype [4] enforce combining both genetic and phenotypic traits to achieve more accurately stratification of melanoma patients. This evidence concerns the gene BRAF and melanoma.