In contrast, it has been reported that IL-17 and tumor-associated macrophages (TAMs) rather than VEGF, contribute to tumor progression; an elevated NLR is correlated with the up-regulation of IL-17 and an increased TAM infiltration into peritumoral regions, by which HCC growth, tumor migration mediated by matrix metalloproteinase, and downregulation of the anti-tumor immune response are induced [28]. The gene discussed is IL17A; the disease is neoplasm.