NFKB1 and neoplasm: On the other hand, a possible mechanism for an anti-tumor function of HDAC3 in macrophages is direct deacetylation of NF-κB (p65/relA), which is associated with overall termination of the NF-κB transcriptional response (93), but specific activation of transcription of the anti-tumor macrophage cytokine, interleukin-1 (IL-1) (94).