Since Cu chelation decreases the Cu dependence of MEK1/2 activation for KRAS [1] or BRAF [2, 3] optimal oncogenic signalling, and U0126 selectively binds and inhibits MEK-1/2 [24] but also protects from oxidative stress [25], we hypothesised that sub-toxic Cu chelation together with UO126 would diminish non-specific toxicity preserving anti-tumour activity against melanoma cells with KRAS or BRAF mutations. The gene discussed is KRAS; the disease is neoplasm.