Our in-depth investigation using the B16-OVA melanoma model revealed that the anti-tumor effect of DB is mediated by enhanced tumor infiltration of cytotoxic lymphocytes, particularly cytotoxic CD8+ T cells, which depends on the increased expression of CXCL9 by tumor-associated macrophages (TAMs) and the CXCL9-CXCR3 chemokine axis. The gene discussed is CXCR3; the disease is neoplasm.