We also show that 17-AAG can suppress both cell proliferation and the paradoxical activation of ERK [21, 22] in NRAS melanoma cells treated with BRAF inhibitor N-(3-(5-(4-chlorophenyl)-1H-pyrrolo[2;3-b] pyridine-3-carbonyl)-2,4-difluorophenyl) propane-1- sulfonamide (PLX4032 or vemurafenib). This evidence concerns the gene BRAF and melanoma.