Our findings concur with the demonstration that in oncogenic RAS-mutant and kinase-dead BRAF-mutant cells, tumor progression is driven through a similar mechanism of c-Raf recruitment and hyper-activation [53] and suggest that BRAF-impaired cancer cells may be as susceptible to therapeutic inhibition of IGF signal transduction as has been proposed for RAS-mutant cells [43, 44]. Here, RAF1 is linked to neoplasm.