Prior studies have either (i) been performed in cells originally lacking mutations in KRAS or BRAF, such as SW48, thus being independent of these mutations for tumor formation [3], (ii) compared KRAS and BRAF mutations in different genetic backgrounds [5, 9], or (iii) been limited to characterizing either the transcriptome, proteome or metabolome without integrative approach. This evidence concerns the gene BRAF and neoplasm.