The oncogenetic tree analysis resulted in a reproducible tree with three branches: (1) The first branch was initiated by the methylation of “methylation in tumor” (MINT) sites, predisposing to MSI, methylation of MLH1 and TP16, and B-Raf mutation; (2) the second branch was initiated by an APC mutation and followed by a p53 mutation; and (3) the third branch was due to a K-Ras mutation and was not followed by any other genetic alteration [31]. Here, KRAS is linked to neoplasm.