A reduction of systemic pro-inflammatory cytokines, mainly TNF and IL-6, in mice treated with B16shR-SOCS1 and down-regulation of NF-κB (p65) in these cells suggest that SOCS1 could favor the epithelial-mesenchymal transition (EMT) leading to tumor progression48, 49. This evidence concerns the gene NFKB1 and neoplasm.