Results obtained in mouse models again reflect the need for well-adjusted DNMT function to maintain cellular homeostasis: DNMT1 knockout mice are ‘protected’ against the development of colorectal adenomas when crossed with APC-deficient mice (Laird et al, 1995), but they are ‘prone’ to develop lymphomas in the context of mice susceptible to this type of neoplasia (Eden et al, 2003). This evidence concerns the gene DNMT1 and neoplasm.