A recent study showed that maintenance of eIF4F, the complex containing eIF4A activated by eIF4E via its interaction with eIF4G6 was the common route for the acquisition of resistance to therapeutic drugs targeting mutant BRAF in melanoma cell lines and patients.36 Furthermore, eIF4A inhibitors showed synergistic effects on cellular proliferation in combination with anti-BRAF therapy. This evidence concerns the gene BRAF and melanoma.