In addition, following systemic chemotherapy, breast and pancreatic CAFs secreted large amounts of the “ELR-motif-positive” (ELR+) CXCL chemokines through chronic activation of the STAT-1 and NF-κB transcriptional activities, which stimulated CXCR-2 signaling in cancer cells to elicit their transdifferentiation into CSCs and thereby promoted post-treatment tumor aggression and treatment failure (37). This evidence concerns the gene NFKB1 and neoplasm.