Gene expression profiling studies mapping the gene signatures downstream of a constitutively activated MAPK pathway suggested that cutaneous melanoma cell lines with NRAS mutations are less dependent in signaling through this pathway compared to BRAFV600E mutant cutaneous melanoma cell lines [10,16], explaining in part the differential sensitivity of NRAS and BRAF mutant cells to MEK inhibitors [7]. Here, BRAF is linked to cutaneous melanoma.