For example, the inhibition of these targets has already been explored on colorectal cancer by means of combination of drugs, as drug resistance that derives by overexpression and activation of EGFR could be overcome through the blockage of B-Raf.20,100 The design of B-Raf/EGFR dual inhibitors has also been probed as a strategy to overcome drug resistance observed on melanoma and colorectal cancers to approved B-RafV600E drugs, providing promising results. This evidence concerns the gene EGFR and melanoma.