AKT1 and melanoma: In ERK-dependent resistance, it has been proposed that the upstream activator protein of BRAF-NRAS is mutated (~20% of NRAS is mutated in melanomas, the most common ones being Q61R/K/L) and bypasses BRAF inhibition via ARAF and/or CRAF, resulting in the reactivation of MAPK signalling pathways [12,35,36,37] as well as that of the PI3K-AKT-mTOR (phosphatidylinositol-3-kinase-protein kinase B-mammalian target of rapamycin) pathway [38].