EVs derived from melanoma cells, for example in vitro, compromise the correct maturation of dendritic cells (DCs) by negatively regulating monocyte maturation (the DCs, in the lymph nodes, are crucial to detect and present tumor-associated antigens to lymphocytes); moreover, EVs treatment of DCs downregulates some chemokines (FLT3L, IL-15, MIP-1α, and MIP-1β) compared with the control, suggesting an alteration of DC functions mediated by melanoma EVs [110]. This evidence concerns the gene CCL4 and melanoma.