Electrophoretic mobility shift assays and transient transfection assays revealed presence of NF-κB binding sites on CXCR4 promoter regions, suggesting that NF-κB may directly regulate the transcription of CXCR4. Similar results were demonstrated in pancreatic cancer cells, where IL-1 induced NF-κB signaling was coupled with the increased co-expression of another marker of stemness—CD133 on cells that were responsible for the formation of aggressive tumors [87]. This evidence concerns the gene NFKB1 and pancreatic neoplasm.