Similarly, when Apc, a key gatekeeper of intestinal tumorigenesis, is deleted in short-lived transit-amplifying cells in colonic crypts using Ah-Cre×loxP-Apc mice, the growth of the induced microadenomas rapidly subsides while inactivation of Apc in long-lived colonic stem cells leads to persistent adenomas [26]. The gene discussed is APC; the disease is adenoma.