Previous studies on BMMSC-derived Ccl2 primarily focused on its paracrine effects on facilitating macrophage recruitment and M2 polarization,68 suppressing CD4+ T-cell activation and promoting myeloid cell differentiation,69,70 enhancing anti-tumor properties in prostate cancer,71 and accelerating wound healing.72 Here, we show that BMMSC-secreted Ccl2 induces Lcn2 production in an autocrine manner, thereby shifting cell commitment from osteoblasts to adipocytes. The gene discussed is CD4; the disease is prostate carcinoma.