Likewise, effects of the pharmacologic inhibition of the CCL8-CCR5 signalling pathway in various cancer models, either with the CCL8 inhibitor Bindarit [85,86], or by inhibiting its major receptor CCR5 by Maraviroc [42,87,88], has been thus far, for the most part, attributed to their complex effects on the tumour microenvironment, e.g., by diminution of cancer-related inflammation and myeloid or suppressor T-cell cell infiltration, or by limiting accumulation of cancer-associated fibroblasts. This evidence concerns the gene CCL8 and neoplasm.