TP53 and neoplasm: The individual actions of NF-κB, STAT3, and AP-1 are insufficient to govern the gene expression programs that sustain tumor-promoting inflammation; crosstalk and cooperative action is important, and interaction with many other transcription factors and associated signaling cascades (e.g., p53, HIF-1α, and WNT-β-catenin) has also been reported [95,100].