Tumor destruction by the prominent neutrophil and macrophage influx mediated by CXCL3 [15–17] overcomes, at least in our setting, its well-known pro-angiogenic effects [14], since microvessel density remained unaltered in AC and slightly decreased in SCC tumors from IL-27-treated animals, when compared with controls. Here, CXCL3 is linked to neoplasm.