This classical model of CRC development assumes the coexistence of several mutations in suppressor genes, such as APC regulator of WNT Signaling Pathway (APC) or tumour protein p53 (TP53), and overlapping mutations of proto-oncogenes, e.g., K-RAS (KRAS proto-oncogene), which activate the critical pathways that determine further progression [10]. The gene discussed is KRAS; the disease is colorectal carcinoma.