The histologic and molecular neoplastic progression of human colorectal carcinoma has been well defined for over 30 years (40), typically beginning with biallelic APC inactivation (to form precursor adenomas), followed by sequential acquisition of activating KRAS mutations and TP53 inactivating alterations, and chr 18q loss during the transition to overt adenocarcinoma. The gene discussed is APC; the disease is adenoma.