NRAS and cancer: Our detailed and targeted sampling of the mutational landscape of BRAF in TCGA melanoma as well as in all other tissues of TCGA by next-generation sequencing brought three main insights forward: a) BRAF is significantly increased at a copy-number level and constitutively activated by somatic mutations; b) The whole-exome data showed unprecedented diverse mutational events within BRAF (Figure 3) aside from p.V600E preserving mutual exclusivity to activating NRAS mutations; c) Other cancers have similar or even stronger BRAF signatures than melanoma.