In our opinion, since the DNA for mutation testing was extracted from a whole biopsy specimen, this finding might be due to the fact that the fraction of KRAS-mutated cells in these precursor lesions might be lower than in a specimen that consists mainly of homogeneous tumor tissue, and Abi1 upregulation upon adenomatous change in major parts of the polyp might mask the stronger Abi1-overexpression in a minor, KRAS-mutated part of the lesion. The gene discussed is ABI1; the disease is neoplasm.