Results of the current in vivo study showed that although intrinsic production of CXCL10 by B16F10 cancer cells contributed to the increase of CXCL10 levels during subcutaneous B16F10 melanoma tumor growth, host-deficiency of CXCL10 almost failed to lead to CXCL10 augmentation (Figure 1(A)) and B16F10 tumor growth (Figure 1(B)), indicating an important role of and the main source of host-derived CXCL10 augmentation induced by interaction between melanoma cancer cells and host-cells or host-microenvironment. This evidence concerns the gene CXCL10 and neoplasm.