Using conditional knockout of BRAF and/or CRAF in a mouse melanoma model induced by NRASQ61K, we showed that while BRAF is required downstream of activated NRAS for tumor initiation, both BRAF and CRAF play compensatory functions during late phases of melanomagenesis, thus highlighting the addiction of melanoma to the RAF/ERK pathway7. This evidence concerns the gene BRAF and neoplasm.