It may be noted that all the pathways listed in Table 2 and Table S6 were dysregulated in CRC tissue compared to normal tissue regardless of whether the tumor had KRAS mutation or was of the wild-type, but for the pathways in Table 2, the magnitude of differential expression was significantly greater in patients with the KRAS mutation than in the KRAS wild-type indicating the association between the KRAS mutation status and gene expression pathways (see the “interaction p” column of Table 2). This evidence concerns the gene KRAS and neoplasm.