Similar to PRL overexpression, CNNM4 knockdown in cultured cancer cells promotes tumor formation in mice, and Cnnm4 disruption in mice heterogeneously deficient in Apc, which are predisposed to have benign intestinal polyps, stimulates malignant progression of the polyps to invasive adenocarcinomas. This evidence concerns the gene CNNM4 and intestinal polyp.