NFKB1 and neoplasm: Prior research had shown that dual stimulation in macrophages via the canonical NFkB (e.g., TLR7/8 agonists such as R848) and non‐canonical NFkB pathway (e.g., cIAP inhibitors) could achieve this.[8] There is further evidence that STAT, PI3Kg, or JAK inhibition could re‐program tumor myeloid cells and potentiate the effect.