In the early stages of MAP tumourigenesis, a dominance of the BER defect can be concluded from the high frequency of G>T tranversions in KRAS2 and APC. In the later stages such G>T transversions seem less prominent, as seen in SMAD4 and p53. Mitotic recombination might be a driving force in MAP carcinogenesis, based on our conclusion that the LOH in MAP carcinomas mainly comprise copy neutral LOH. The gene discussed is APC; the disease is carcinoma.