Previous studies targeted to ascertain the molecular progression of CRC investigated genetic abnormalities of proto-oncogenes (K-Ras) and tumour suppressor genes (p53 and APC) or, alternatively, molecular epigenetic changes (E-Cadherin, p16INK4A, DAPK, RASSF1A and APC) (Smith et al, 2002; Lee et al, 2004). The gene discussed is KRAS; the disease is colorectal carcinoma.