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Patients with familial adenomatous polyposis (FAP) have inflamed colons and have a high risk of colon cancer. These patients have defective retinoic acid (RA) metabolism that produces a local deficit of RA in the tumor milieu. Using a mouse model of FAP, decreased or absent RA encouraged disease progression, but inhibiting an enzyme that catabolizes RA ameliorated disease. One of the effects of increasing RA was to dampen the inflammatory phenotype of gut dendritic cells, and these cells were found to be crucial for adenoma formation. Read more in the article by Penny and colleagues starting on page 917 of this issue. The confocal microscopy image is of an FAP polyp, with red labeling an inhibitor of the RA metabolic pathway, CTBP1, and green denoting dendritic cells labeled with DC-SIGN (photo by HL Penny, of the Edgar G Engleman lab). Artwork by Lewis Long.