Because mutated B-RAF leads to constitutive activation of the mitogen-activated protein kinase pathway (MAPK) that, in turn, increases the cellular proliferation and drives the oncogenic activity [29, 30], intensive research has consisted to selectively inhibit mutated B-RAF in patients with melanoma (e.g., studies with sorafenib, a multitargeted kinase inhibitor), but the results were globally disappointing due to off-target side effects mainly induced through inhibition of wild type B-RAF [14, 31–35]. Here, BRAF is linked to melanoma.