Through these angiogenic effects, recombinant SLIT3 was found to have therapeutic activity in mouse models of fracture healing and postmenopausal osteoporosis.8,15 Meanwhile, a separate study reported that SLIT3 is critical for skeletal physiology and also found osteopenia and a reduction in the skeletal vascular endothelium in Slit3−/− mice.9 However, in this report, osteoclasts, as opposed to osteoblasts, were nominated as a key source of SLIT3 to control coupling between osteoblasts and osteoclasts. This evidence concerns the gene SLIT3 and postmenopausal osteoporosis.