Overexpression of BRAF in melanocytes potentiated β‐Trcp expression and NF‐κB activity, while inhibition of either BRAF or downstream MEK led to the reduction in β‐Trcp expression and NF‐κB activity, proving that the hyperactivated BRAF‐MEK signaling cascade in melanoma sustained NF‐κB activation through the up‐regulation of β‐Trcp expression 82. This evidence concerns the gene BRAF and melanoma.