However, further work will be required to understand why the 14-3-3-binding deficient form of PAK4 is more effective than wild-type PAK4 in supporting the melanoma cell phenotype, particularly given that roles have been identified for PKCs, including PKCδ, in survival and metastatic invasion of melanoma cells carrying RAS and BRAF driver mutations [12,55–62]. This evidence concerns the gene BRAF and melanoma.