Our study revealed that blocking the transcriptional activity of HIF-1α, by disrupting HIF-1α/HIF-1β dimerization, significantly inhibited B16-F10 melanoma growth and increased the infiltration of NK and CD8+ T cells into the tumor microenvironment by a mechanism involving the release of CCL2 and CCL5 chemokines. Here, CCL2 is linked to neoplasm.