Both clinical and preclinical researches focused for decades on the role of “adenomatous polyps” as cancer precursors; the adenoma-carcinoma sequence, involving the accumulation of different progressive genetic mutations (APC, K-RAS, DCC, and p53), is widely recognized, and around 50-70% of CRC arises from conventional adenomas and is “microsatellite stable” [2]. The gene discussed is TP53; the disease is adenoma.