Heterozygous deletion of Apc drives the formation of adenomas (benign tumours) and microadenomas (very small tumours not visible to the naked eye – examples of histology are provided in the supplementary material, Figure S4A) in the small intestine of mice with a long latency; combining Apc loss with expression of mutant KRasG12D accelerates this progression by around three‐ to four‐fold 34, 35. The gene discussed is APC; the disease is neoplasm.