Although this study is still at an early stage, our results suggest that mutant KRAS/high c-MYC amplification [38] may change the anti-tumour response to some specific Cu chelators in wt p53 C8161 and A375 melanoma, which are compatible with others who found that c-MYC deregulation without elevated expression cooperates with KRASG12D mutation to accelerate tumourigenesis [35, 36, 38]. The gene discussed is TP53; the disease is neoplasm.