After the establishment of an inflammatory TME through IFN networks, tumor cells gain STAT3 activity through immune-derived IL-10, IL-6, NF-κB, or Bcl2, which promote proliferation, antiapoptotic signals, and angiogenesis and additionally, these secreted factors drive expansion of MDSCs and Tregs, which, together with macrophages and DCs, produce immunosuppressive TGF-β and IL-10 cytokines and also express other immunoregulatory molecules, including arginase, inducible NO synthase, and IDO (82, 83). Here, NFKB1 is linked to neoplasm.