BRAF and neoplasm: Collectively, this data suggests that by disregarding the in vogue approach of using highly specific kinase inhibitors for personalized medicine approaches against a specific clonal tumor cell type, e.g. the dabrafenib/trametinib combination against mutant B-RAF, we have been able to out-fox both the evolutionary survival responses of tumor cells as well as being able to kill tumor cells carrying a wide variety of upstream mutations that would predict for drug resistance and a shorter overall patient survival.