In vitro work suggested that HIF-2α is suppressed at 3′UTR by miR-17 and miR-20a and treatment with tumor cell supernatant or autocrine-derived IL-6 abrogates miR-17 and miR-20a-mediated suppression of HIF-2α in healthy peripheral blood monocyte-derived macrophages in an oxygen-independent manner suggesting, despite being a pro-inflammatory cytokine, that pleiotropic IL-6 can preferentially induce macrophage HIF-2α, indirectly [108]. This evidence concerns the gene IL6 and neoplasm.