Each cell typically contains several hundred of a special class of enhancers that stretch over many kilobases long DNA sequences, called "super-enhancers". These enhancers contain a large number of binding sites for sequence-specific, inducible transcription factors, and regulate expression of genes involved in cell differentiation. During inflammation, the transcription factor NF-κB facilitates remodeling of chromatin in a manner that selectively redistributes cofactors from high-occupancy enhancers, thereby repressing genes involved in maintaining cellular identify whose expression they enhance; at the same time, this F-κB-driven remodeling and redistribution activates other enhancers that guide changes in cellular function through inflammation. As a result, inflammation reprograms cells, altering their interactions with the rest of tissue and with the immune system. In cancer, proteins that control NF-κB activity are dysregulated, permitting malignant cells to decrease their dependence on interactions with local tissue, and hindering their surveillance by the immune system.