We also show for the first time that the synergism between sub-lethal levels of DSF and the highly specific MEK inhibitor UO126 [24] against melanoma cells, irrespective of BRAF or KRAS/c-MYC status, This synergism may be partly explained by DSF chelating activity sequestering Cu [21] required as a MEK1/2 co-activator in KRAS-[1] or BRAF-mediated oncogenic signalling [2, 3] and MEK inhibitors like UO126 [24] directly binding to MEK1/2. This evidence concerns the gene BRAF and melanoma.