There are two distinct molecular pathways involved in CRC development; one is the traditional adenoma–carcinoma pathway, which is associated with chromosomal instability and mutations in specific tumor suppressor genes and oncogenes (e.g., APC, RAS, and TP53), and the other is the serrated pathway, which involves the CpG island methylation phenotype and microsatellite instability [4]. The gene discussed is TP53; the disease is colorectal carcinoma.