Three major genetic mechanisms have been reported to be involved in early CRC and precancerous colorectal lesions: (1) chromosomal instability due to mutations in APC, KRAS, and TP53; (2) microsatellite instability due to a loss of function in mismatch repair genes; and (3) DNA methylation, which is an epigenetic alteration leading to promotor hypermethylation and subsequent suppression of gene transcription [33]. The gene discussed is TP53; the disease is colorectal carcinoma.