Animal models of prostate cancer osteoblastic bone macrometastasis derived from hematogenous spread of tumors do not presently exist despite many attempts[43–47], but our findings suggest the idea that genetically engineered models of prostate cancer harboring overexpression or amplification of osteopontin, OB-cadherin, SPARC, RANKL, or osteocalcin or deletion of RUNX2 may lead to osteoblastic bone metastases. This evidence concerns the gene RUNX2 and prostate carcinoma.