Some abnormalities such as gain of chromosome 12 (presence of the pluripotency NANOG gene and the cell-cycle regulator CCND2 in 12p13; the oncogene KRAS in 12p12.1), chromosome 17 (BIRC5 candidate gene in 17q25, an antiapoptotic gene associated with the highest-risk tumor), chromosome 20 and chromosome X or fragments of these chromosomes may promote self-renewal and thus provide a selective proliferative/survival advantage [3,31,32]. This evidence concerns the gene KRAS and neoplasm.