These results are in concordance with those of Marx et al. Using Laser-capture-microdissection Zhang et al. discovered different deletions in the AMACR promotor CpG Island, depending upon the underlying tissue: In normal colonic glands and tubular adenomas with low AMACR expression they detected a somatic double-deletion at CG3 and CG10, that was absent in villous adenomas and all colon cancers with variable AMACR levels. Here, AMACR is linked to villous adenoma.