The proliferation of cells with an unstable genome is accompanied by the development of aneuploidy, which is observed in 65-85% of sporadic colorectal tumors (35-38), and is often accompanied by mutations in the adenomatous polyposis coli (APC), tumor protein p53 (TP53), catenin beta-1 and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha genes, in 20% of cases (39). This evidence concerns the gene APC and colorectal neoplasm.