Interestingly, these authors found that the effects of curaxins on p53, NF-κB, and their toxicity to cancer cells result from “chromatin trapping” of the histone chaperone FACT (facilitates chromatin transcription) complex; and the FACT inaccessibility leads to phosphorylation of the p53 Ser(392) by casein kinase 2 and inhibition of NF-κB-dependent transcription, which requires FACT activity at the elongation stage [144]. Here, TP53 is linked to cancer.