Last, in-vitro work showed that resistance to B-RAF inhibition could be overcome by simultaneously co-targeting MEK and IGF1R/PI3K, and that indeed IGF1R levels are increased in human tumor sample following the acquisition of resistance to B-RAF inhibition, consistent with a role for IGF1R/PI3K-dependent survival in the development of such resistance [42]. This evidence concerns the gene IGF1R and neoplasm.