In summary, we demonstrated that BCC‐Ex differentiated the bone marrow cells into MDSDs and inhibited the proliferation of T lymphocytes in vitro and in vivo and the possible mechanisms may be related to BCC‐Ex‐mediated the activation of STAT3 signal pathway and down‐regulation of the expression of chemokine receptor CXCR4. Obviously, elucidation of the mechanism of BCC‐Ex on MDSCs generation should provide an insight into the development and immunotherapy of breast cancer. The gene discussed is STAT3; the disease is breast cancer.