Indeed, our previous study demonstrated that prostate carcinoma–produced PDGF D induces osteoblastic bone reactions and promote intraosseous tumor growth in mice and that treatments with cediranib (an inhibitor of PDGFR/vascular endothelial growth factor receptor) significantly reduced the trabecular bone levels (∼75% reduction) ((20, 21) and Fig. S1). This evidence concerns the gene PDGFD and prostate carcinoma.