The Min mouse, generated by random germline mutagenesis, carries a mutation in the mouse homolog of APC and is a model of inherited human intestinal tumorigenesis. To identify other genes in the pathway(s) of intestinal tumorigenesis, genes that modify the Min phenotype have been sought. Several have been identified, including Mom1 and the genes for the 5-cytosine DNA methyltransferase and the DNA mismatch repair factor Msh2. Min-dependent tumorigenesis also occurs in mammary glands, the pancreas, and the body wall. The Min mouse has therefore become a model for tumorigenesis in a variety of organs. Identifying modifiers of its phenotype will help in piecing together the pathways of tumorigenesis in each of these tissues.