This shift from CCL5/CXCL9/CXCL10 to CXCL8/CXCL12/CCL22 production was attributed to NFκB-mediated induction of COX2/PGE2/EP4, along with upregulation of IDO1 and IL-10, further contributing to the immunosuppressive tumor microenvironment [187,188]. The gene discussed is NFKB1; the disease is neoplasm.