Two major and mutually exclusive types of genomic instability are involved in cancer progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes, including activation of oncogenes and inactivation of tumor-suppressor genes such as p53 and APC. The second, known as microsatellite instability (MSI), results from somatic (acquired) inactivation of DNA mismatch repair genes (MMR), such as MLH1 (by hypermethylation of its promoter), typically leading to mutation of genes with coding microsatellites, such as BAT 25, BAT26 and CAT25, transforming growth factor receptor II (TGF-RII) and BAX [6].