Since both KRAS and BRAF mutations drive tumour cell proliferation by Cu-dependent MEK1/2 kinase activation through different responses in melanomas [4] or colorectal carcinomas (CRC) [5], we also studied the response to TTM and/or DSF in mutant p53 CRC with mutant KRAS [29] and high c-MYC [30] compared to CRC cells with a BRAF-mutant [29] low c-MYC [30] status and another mutant p53 CRC harbouring wt BRAF and wt KRAS [29]. This evidence concerns the gene MYC and neoplasm.