CRC represents a heterogeneous group of cancers arising through different combinations of genetic and epigenetic events [2]: the “conventional” pathway to CRC is characterized by adenomatous polyposis coli (APC) mutation, chromosomal instability, and paucity of CpG island hypermethylation, while the “serrated” pathway is characterized by B-Raf proto-oncogene, serine/threonine kinase (BRAF) mutation, chromosomal stability, and high CpG island hypermethylation [3]. This evidence concerns the gene MARK2 and colorectal carcinoma.