Adoptive transfer of CIK to tumor-bearing mice induced an increase in inflammatory mediators (e.g., CX3CL1, IL-13) and tumor-infiltrating MDSC in the tumor microenvironment, and MDSCs effectively inhibited the cytotoxic activity of CIKs in vitro. In contrast, treatment with PDE5 inhibitors reversed MDSC inhibition by Arg1 and iNOS, while systemic treatment with PDE5 inhibitors prevented MDSC accumulation in the tumor microenvironment after CIK cell treatment and increased its anti-tumor efficacy. This evidence concerns the gene CX3CL1 and neoplasm.