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Mutant embryos exhibited aortic and pulmonary valve stenosis due to semilunar valve thickening, with occasional ventricular septal defects. Semilunar valve mesenchymal cell proliferation increased in mutants from embryonic day 14 onward, but the cell death rate remained unchanged. <jats:italic>Cxcr7<\/jats:italic> mutant valves had increased levels of phosphorylated Smad1\/5\/8, indicating increased BMP signaling, which may partly explain the thickened valve leaflets. The hyperproliferative phenotype appeared to involve <jats:italic>Cxcr7<\/jats:italic> function in endocardial cells and their mesenchymal derivatives, as <jats:italic>Tie2\u2010Cre Cxcr7<\/jats:italic><jats:sup><jats:italic>flox<\/jats:italic>\/\u2212<\/jats:sup> mice had semilunar valve stenosis. Thus, CXCR7 is involved in semilunar valve development, possibly by regulating BMP signaling, and may contribute to aortic and pulmonary valve stenosis. 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