Chemokines are small soluble molecules that are best known for their potent ability to induce cancer cell growth by inflammation. Many types of cancer cells express chemokines and chemokine receptors [1]. The accumulated evidence indicates that the chemokine (C-C motif) ligand 5 (CCL5) and C-C chemokine receptor (CCR5), which are potent chemotactic factors for inflammatory cells, may be significantly involved in the proliferation and metastasis of several cancers. Intermediate and strong CCR5 expression is significantly associated with nonmetastatic development of colorectal cancer [2], melanoma [3], hepatoma [4], glioblastoma, Hodgkin lymphoma [5], as well as oral and prostate cancer cells [6]. Local production of the CCL5 is also important in the progression of breast cancer [7], and also correlates with poor prognosis [8]. Meanwhile, CCR5 disruption has been demonstrated to inhibit experimental tumor growth and metastasis of pancreatic cancer [9]. In addition, host absence of CCR5 potentiates the delay of tumor growth [10], and CCR5 inhibitors prevented cancer cell growth, such as prostate cancer [11], breast cancer, hepatoma cells [4], and lung cancer [12]. These data suggest that the deficiency of inflammatory chemokine receptor CCR5 may function as a suppressive receptor in cancer progression. However, more studies are required to describe how CCR5 deficiency acts in the inhibition of tumor development.